Cold War

Cold War “Super-Pleasure”:

Insatiability, Self-Stimulation, and the Postwar Brain by Otniel E. Dror[1]


In this contribution, I study the post-World War II discovery of a new “supramaximal” “super-pleasure” in the brain. I argue that the excessiveness of the newly discovered supramaximal super-pleasure challenged existing models of organisms, of the self, and of nature and society, and that it prescribed a rethinking and a repositioning of pleasure. I reconstruct the laboratory enactments and models that constituted this new pleasure as “supramaximal,” instant, and insatiable, suggest several postwar contexts that situate the new pleasure, and examine expert and vernacular reactions to the new super-pleasure. I also introduce and reflect on an approach that “sides with” emotion, and I present the notion of a “missed” emotion. I conclude with a brief consideration of “repetitions”–for science and for pleasure.

A system (the fornix system) in the so-called “olfactory” part of the brain is in some way involved in intensely pleasurable activity.

–John C. Lilly, 19551

Among the most recently discovered is a region within [the hypothalamus] . . . which on stimulation gives rise to a strongly pleasurable sensation. . . . Evidently all the desirable things in life are desirable only insofar as they stimulate the pleasure center. To stimulate it directly makes all else unnecessary.

–Isaac Asimov, 19652

For the first time in the history of neuroscience, this arrangement enabled an animal to push a lever and deliver a stimu-


lus–in this case, obviously, reinforcing and, presumably, pleasurable–to the interior of its own brain! The later popular term for this behavior–“self-stimulation”–was introduced by Joseph V Brady in 1958.

–H. W. Magoun, 1981[2]

In 1954, James Olds and Peter Milner discovered pleasure in the brain of a laboratory rat. Pleasure, which had been ostracized as a nameable experience by the behaviorist sciences, which had been de-ontologized during the early twentieth century as merely aponia–as only an absence of pain–and which had been excluded from the repertoire of possible states of laboratory animals since the early inauguration of a laboratory science of emotions during the nineteenth century, returned with a vengeance.[3] The return of pleasure introduced a major transformation whose repercussions and offshoots are still very much with us today, including the development of a neurophysiology of decision making, risk taking, addiction, affective neuroscience, and more.

The history of the discovery of pleasure during the mid-twentieth century intertwined with numerous historical developments and contemporaneous contexts. Some harked back to classical times, like the long history of Western hedonisms. Others emerged in their modern guise during the eighteenth century: in Kantian aesthetics, and in the aesthetics of Burke and Hume; in the hedonisms of Thomas Hobbes and Robert Whytt; in Bentham’s “pig’s philosophy”; and in what Colin Mercer has defined as the eighteenth-century “individualisation of pleasure . . . the first stage in the introduction of individual pleasures into the field of documentation and social regulation.”[4] Other developments occurred during the decades that immediately preceded the return of pleasure, like the rise of behaviorism and the praxis of (deep) brain stimulation. Still others emerged contemporaneously, including the significant and interrelated development of behavioral or psychopharmacology. The emergence of pleasure also coincided with the anxieties of the Cold War and the development of a unique “Cold War rationality” (which was distinct from “reason”), the negation and “pathologization of emotions” in the post-Holocaust social sciences of liberal democratic societies, and the approaching horizon of the long sixties (1958-74). Freudian- ism was still thriving in the United States, and post-Freudian adaptations, reinterpretations, and critiques appeared in the works of Herbert Marcuse, Norman O. Brown, Betty Friedan, Jacques Lacan, and Ernest (ne Ernst) Dichter.[5] Into this melee of cultural forces, contradictions, and ideologies, scientists introduced “supramaximal” “superpleasure.”

In this contribution, I study the discovery of super-pleasure during the mid-twentieth century.[6]1 partly adopt the suggestion made by Edward Boring in the mid-1920s, when the National Research Council convened a confidential Committee and Conference on the Experimental Study of Human Emotions: “the first thing to do,” Boring suggested, “is to bring together all the people who are working on emotion and let them tell what they are doing. . . . Then you will find out what in the world emotion is that can be investigated.”[7] In adopting Boring’s suggestion, I follow experimenters who encountered pleasures inside their laboratories. Rather than providing a close reading of a particular development or laboratory, I present a broad perspective in characterizing the new brain super-pleasure of the immediate postwar period.[8]1 focus on the first decade or decade and a half following the discovery of the new pleasure. This early period was characterized by multiple models and hypotheses, incongruent and conflicting terminologies and ideologies, and an intensive empiricism.

In describing the discovery of pleasure, I do not present a “balanced” history. Rather, I “side with” pleasure in a broader behaviorist context, in which “pleasure”–the very word–was often derided, obfuscated, and maligned. Pleasure often had to make itself heard, after an absence of several decades. My first intention in siding with pleasure is thus to empower this underdog emotion. This historiographical choice is significant,

6     On Cold War rationality, see Paul Erickson, Judy L. Klein, Lorraine Daston, Rebecca Lemov, Thomas Sturm, and Michael D. Gordin, How^eason^lmost^ostJts^ind:The^trange,CarSSLSf since the allusion or nonallusion to “pleasure” was–and still is–highly contentious for many investigators. It reflected methodological and ideological distinctions that permeated the discovery of super-pleasure and also permeates my analysis below.

In siding with pleasure and presenting a narrative that takes off from “emotion,” I also indicate that “pleasure” in my narrative was not the doppelganger–or evil twin– of scientific “reward,” as many investigators conceived–and still conceive–“pleasure.” Pleasure was not an afterthought, a misspoken term and presence, a puerile throwback to be regretted in retrospect (by behaviorist scientists), or a layperson’s misapprehension of science. “Pleasure” was significant for its scientific history, for the history of scientific “pleasure,” from its very beginning. It was also highly significant for the scientific history of “reward.”

Siding with pleasure also highlights the alternative narratives that become available from a history-of-emotions perspective. As I will argue below, the discovery of the new pleasure evoked and invoked a broad angst at the very moment of its emergence. “Reward,” on the other hand, was exempt from these connotations. There was no angst associated with reward. There was no ostensive affective charge to the discovery of reward in the brain. Furthermore, and significantly, there was “super-pleasure” and “supramaximal” pleasure, but there was no “super-reward” or “supramaximal re- ward”–there was just “reward.” In addition, “pleasure” and “reward” harked back to different histories and presented divergent meanings, associations, and connotations. A history in terms of “pleasure” and a history in terms of “reward” present two alternative narratives of the exact same developments–of the exact same discoveries, experiments, laboratories, technologies, investigators, and rats. Here, I let pleasure be heard.[9]


Dr. Marianne E. Olds remembered the day of the discovery of pleasure in the brain:

At the time no one ever expected that the brain had reward sites, and not that reward was simply the absence of pain. My husband who came from a deeply religious family was not very familiar or had ever seen individuals taking rats, drilling holes in their brains and putting in twisted wires whose ends had been scraped very, very slightly. The result was very poor surgery, the electrode was placed at a site where the reward was very minimal which was lucky because the rat did not go crazy with pleasure but was sufficiently activated to come back, time and time again, to the site where my husband was testing him.. . . The upshot was Jim Olds coming home that Sunday and saying that he had discovered the pleasure center.[10]

The discovery of pleasure in the brain was the immediate effect of the rapprochement of behaviorism with neurophysiology and serendipity. There are several versions of the renowned story of the discovery of pleasure-reward in the brain. The main thread of the discovery story is as follows: James Olds, a recent Harvard PhD in social psychology and an advisee of Talcott Parsons, was a new postdoc in Donald O. Hebb’s laboratory at McGill University. Hebb’s laboratory was one of the first major centers that integrated psychology-behaviorism with neurophysiology.[11] One basic methodology in this emergent, bifurcated, and schizoid field was the electrical stimulation of deep–subcortical–regions in the brain, coupled with behaviorist methodologies and conditioning. The stimulation of deep structures in the brain reflected a major and significant shift from a previous focus on the neocortex to a new focus on subcortical structures in explaining complex behaviors.[12] Olds, who had no previous experience in brain physiology, was assisted by Peter Milner, a graduate student in Hebb’s laboratory. One fateful day, after inserting electrodes into a rat’s brain, Olds observed that his brain-stimulated rat seemed to seek the location in the cage where its brain had been stimulated: the “animal could be ‘pulled’ to any spot in the maze by giving a small electrical stimulus after each response in the right direction. This was akin to playing the ‘hot and cold’ game with a child.”[13] Convinced that the rat was “rewarded,” rather than punished, by the electrical shock to its brain, Olds concluded that he had discovered a reward-pleasure site in the brain. Olds immediately realized that his discovery directly challenged the reigning and dominant “drive-reduction” theory and paradigm of motivation (see below). “Jim had a movie made in case it never happened again” and refused to “sacrifice his rat to find out where the electrode had gone,” fearing that his one-of-a-kind rat might be irreproducible. An X-ray of the rat’s brain revealed the true (mis)placement of the electrodes. Together with Milner and Seth Sharpless, another graduate student in Hebb’s laboratory, Olds eliminated alternative explanations for the rat’s behavior in establishing the reality of a true reward-pleasure site in the brain.[14]

Reports of Olds’s discovery spread quickly in the professional and vernacular literatures. Several major researchers were skeptical at first. Among them was Neal E. Miller of Yale University, perhaps the leading protagonist of the drive-reduction theory. Miller, for example, proposed that Olds had not observed a true reward on stimulating the rat’s brain, but an “itch”-like addictive reaction. As Miller explained, each stimulus had “an aversive after effect–something like an itching,” and the rats pressed the stimulating lever a “second time, and a third, and so forth, much in the way one scratches a mosquito bite.”[15] Within a very short period, these objections and alternative explanations were excluded until only pleasure-reward was left.[16]

The discovery of “pleasure” and its discovery in the brain reframed the neurological self.[17] The neurological self was a pleasure seeker, rather than a drive-pain- tension-excitation-need-desire reducer. The new science shifted to a framework of pleasure seeking, “excitement” seeking, and the “good life,” in rejecting the prewar framework in which “pleasure ceased to be a drive in and of itself and was conceived as the experience which occurs when a drive, or motive, terminates, i.e., is satisfied, relieved, or fulfilled.”[18] According to Abraham Maslow, “practically all historical theories and contemporary theories of motivation” regarded

needs, drives, and motivating states in general as annoying, irritating, unpleasant, undesirable, as something to get rid of. . . need reduction, tension reduction, drive reduction, and anxiety reduction. . .. The drive or need presses toward its own elimination. Its only striving is toward cessation, toward getting rid of itself, toward a state of not wanting. Pushed to its logical extreme, we wind up with Freud’s Death-instinct.[19]

This dominant (“drive-reduction”) framework, in which pleasure was only a “negation of a negation” and whose roots hark back to Plato’s Philebus and to Epicurian aponia, was championed by Freud and Hull during the first half of the twentieth century.[20]

Pleasure was (re)-endowed with an independent identity, history, and narrative. It was henceforth an ontological and independent principle in the materiality of the brain substance. It had its own special neurons, its distinct neural matrix, and its own “centers”–soon to be reconceived in terms of “pathways,” and soon thereafter in terms of “circuits.”[21] The brain, moreover, was wired for pleasure. Experimenters determined that the volume of brain stuff that embodied– or rather cerebrated–pleasure was much larger than the volume of brain stuff that cerebrated pain (35 percent for pleasure vs. 5 percent for pain, according to early measurements).[22] These cumulative discoveries also conferred an independent evolutionary history on pleasure, and they reconfigured the interrelationships between pleasure and pain. Pleasure had come into its own, although Gilles Deleuze (among others) would later lament its vacuousness, writing, “I cannot give any positive value to pleasure, because pleasure seems to interrupt the immanent process of desire.”[23]


The discovery of pleasure between behaviorism and neurophysiology bequeathed a split personality to pleasure and to reward. From the very moment of its inception, creation, and discovery, pleasure-reward was haunted by this tenuous duality. Pleasure- reward appertained to two distinct and (often) incongruent epistemologies and ideologies. Pleasure was anathema to behaviorists, like Miller, Larry Stein, and Roy Wise, yet it appeared in the writings of many prominent investigators, like Olds, John C. Lilly, and C. W. Sem-Jacobsen. This is one of the conundrums and ambiguities of referring to pleasure and/or to the behaviorist reward (and “positive reinforcement”) in a semantic field whose members sometimes explicitly referred to pleasure, while at other times obstinately refusing to use the word “pleasure.” Their work was referred to by other scientists and in numerous vernacular literatures in terms of “pleasure,” while a significant, though far from absolute, number of its practitioners rejected “pleasure” and clearly distinguished between pleasure and the behaviorist’s reward and positive reinforcement.[24] For this behaviorist group, reward and pleasure were not interchangeable: a reward was not necessarily pleasurable at all. Reward, moreover, indicated for many the energizing of a drive, in addition to its reinforcing dimensions. “Pleasure” talk, from their perspective, was a return to a preobjective and puerile phase in the development of modern objective psychology.[25]

Nevertheless, pleasure often trumped and usurped reward. John C. Lilly, one of the prominent early leaders of the new neurophysiology, referred to the discovery of brain reward in terms of the “intensely pleasurable.”[26] Olds, who inaugurated the new field, referred time and again to pleasure, including in his 1958 Science article.[27] Other contemporary and prominent investigators, like Maslow, David C. McClelland, and Eliot Stellar, also referred to Olds’s discovery in terms of pleasure.

This “pleasure” challenge was not the product of deliberate attempts to overthrow behaviorism, nor was it an outcome of the infiltration of behaviorism by the ideology and language of animal protection leagues. Rather, it was the result of multiple and local factors: the conjoining of a Skinnerian paradigm with the study of the internal physiology of the brain (Skinner had explicitly excluded a neurophysiology of behaviorism in his 1938 The Behavior of the Organisms);[28] the influx of investigators who had no prior commitments to a strict behaviorist paradigm into this emergent field, including Olds, its founder, and Lilly, one of its major pioneers (these pioneers sometimes used the terms “pleasure” and “reward” interchangeably); the close interactions and collaborations between behaviorists and investigator-clinicians who studied human subjects. These investigator-clinicians, including Robert G. Heath and C. W. Sem-Jacobsen, continuously referred to the subjective experiences of their human subjects, in comparing animal rewards or pleasure to human testimony. They infused and confused introspective human reports of “pleasure,” “joy,” “well-being,” and so forth with the behaviorist (and animal-focused) language of “reward” and “positive reinforcement.” The vernacular literature also converted “reward” talk into “pleasure” talk. In newspapers and magazines, popular-science publications, and (science) fiction, “rewarded” rats and the neurophysiology of “reward” became “pleasure” or “ecstasy.”[29] Philosophical and legal interrogations of these discoveries also referred to the new science in terms of pleasure. In the postwar United States, the science of reward was usurped by pleasure–by the pleasure of (mis)-speaking of “pleasure” and sex and “orgasms” (see below), rather than in terms of the behaviorist’s “positive reinforcement” and “reward.”

Behaviorism played a crucial–even if unwitting–role in this turn to pleasure. Though behaviorism is often credited with (or discredited for) eliminating emotion talk, it provided a crucial ingredient for the science of pleasure and, in particular, for an animal science of “pleasure” (and emotions). Behaviorism authenticated by distinguishing, in terms of behaviorist precepts, between a “psychologically valid reward” and “merely a sham, having the appearance but not the substance of a positive emotional effect” in animals.[30] Behaviorism solved on its own terms the long-standing problem of studying emotions in animals: by getting rid of emotions, on the one hand, but also by formulating authenticating practices for its notion of emotion, on the other hand. Behaviorism provided the necessary tools for identifying and authenticating its version of real emotions (and distinguishing between real emotions and mere motor- reflex movements in animals). This distinction was crucial for the study of drives and rewards, including in the brain.[31] Many “pleasure” investigators depended on the behaviorist’s proof of authenticity (of “reward” in animals) but substituted the be- haviorist’s reward for pleasure. Pleasure thus partly conformed to the logic of the behaviorist’s reward–despite being pleasure–and behaviorism partly prescribed the possibilities for and of pleasure in laboratories, despite being behaviorism. Behaviorism was thus also partly responsible for animal pleasure in the postwar history of animal emotions.[32]

The alter ego of pleasure-reward, neurophysiology, also partly prescribed the nature of reward-pleasure. Neurophysiological pleasure was studied in and confined to the nerves. It conformed to the physiological laws of nerve cells–like the all- or-none principle or the refractory period of nerve cells. These laws prescribed the interpretation of experiments on pleasure.[33] The shift to the brain also disembodied pleasure, but it did not spiritualize it; sometimes it aestheticized pleasure. The cerebration of pleasure, its materialization in terms of brain substance, stripped pleasure of its fleshiness, of its extensions in the body, and of its sensuousness. Pleasure was devoid of drools, secretions, contractions, and spasms, and of their temporal logic, progression, and reverberations in the experienced-felt matter of the body.

Pleasure was studied henceforth in its point of origin in the brain: before it was inhibited, controlled, civilized, and socialized by the internal mechanisms of the brain and of society; before it was distorted and corrupted; before it corrupted and distorted– pleasure in its “pure,” “supramaximal,” and unadulterated form.[34] This ostensibly unnatural laboratory pleasure, which was immediately recognized as such, was the basis for the study of all natural pleasures.


Pure supramaximal super-pleasure was the immediate effect produced by experimental enactments. These enactments made pleasure, and they made it supramaximal. They drew on the behaviorist’s toolbox. They included crossing electric-pain grids, solving mazes, making preference choices, and pressing levers in order to receive an “electrical brain stimulation” (EBS). Their multiplicity thwarted attempts to establish a common denominator or even an agreed-upon value of and for pleasure-reward.[36] Despite their multiplicity, the new pleasure-reward materialized most ostensibly and predominantly in the image and laboratory enactment of the insatiable self-stimulating rat. The insatiable self-stimulating (male) rat pressed a lever that stimulated its own brain’s “pleasure centers” at a rate of up to 8,000 (sometimes even 10,000) presses per hour, forsaking food, water, sleep, and sex (a female rat in heat) –until it collapsed from exhaustion, convulsed, or even died.[37] “He” was soon joined by the insatiable self-stimulating monkey, dolphin, rabbit, goldfish, dog, chicken, and human: “If the tip of a fine wire electrode is placed in a specific area of the brain and a brief, weak electrical current introduced . . . [a monkey] will respond as though he liked the sensation. In fact, if the circuitry is arranged so that he can press a bar to induce the current for a moment, he will press the bar steadily 3 times a second for 16 hours a day, seven days a week for years. Special arrangements must be made to keep the animal from starving or thirsting to death.”[38] There was a report of a dolphin that pushed the lever “too rapidly, [which] caused a seizure, [and then the dolphin] became unconscious, respiration failed, and he died.”[39]

The new super-pleasure was self-perpetuating, self-rewarding, and self-reinforcing. It was produced instantly, on demand, and it dissipated instantaneously. It did not have a refractory period, and it did not lead to satiation. In terms of the “newer information theories,” it was a “positive feedback mechanism” and therefore demanded “external control” (in contrast to the “negative feedback” of drive reduction).[40] Pleasure had to be controlled from outside and beyond itself since pleasure begot pleasure begot pleasure. Science had designed/discovered aperpetuum-pleasure-mobile.

The perpetuum-pleasure-mobile drew directly on previous conditioning experiments. In these experiments, an animal in a Skinner box would receive, for example, a food pellet after pressing a lever. As Olds explained, “By putting the animal in the ‘do-it-yourself ’ situation (i.e., pressing a lever to stimulate its own brain) we could translate the animal’s strength of ‘desire’ into response frequency, which can be seen and measured.”[41]

The scientific and social power and potency of the perpetuum derived foremost from its numerical, experiential, and cultural excessiveness. On the shop-floor level, the excessiveness of the perpetuum challenged investigators, who initially failed to keep up with the rats. Counting individual lever presses of the indefatigable rats “would have taken months, possibly years,” Milner recalled of the first discovery, so the measurement of “the self-stimulation performance [was] by using the length of time a rat was pressing at more than a criterion rate.”[42] This partly explains why “pleasure”- “rewardiness” was not represented in absolute and discrete counts of lever presses, but in terms of rates. The uncountable nature of a super-pleasure on the shop-floor level collapsed a discrete number system for counting the perpetuum. Elliot S. Valenstein, one of the leading investigators of reward and EBS, also presented the excess of the perpetuum in recalling an experiment in which a “rat self-stimulat[ed] for 21 days during which time it operated the switch about 850,000 times…. There was no indication that the animal would ever break the pattern, and it was only the fatigue of my associate, Dr. Bernard Beer, and myself–we were taking turns observing the animal around the clock–that finally forced us to end these observations.”[43]

These failures to count in the face of the perpetuum were partly products of the design of the lever press itself.[44] Because the experiments depended on escalating numbers, rats were compelled to release the lever within 0.5 second in order to receive the next train of brain stimulations. If the rat persisted and continued to press the lever, the current was automatically turned off. This guaranteed that the rat would have to press again in order to receive brain stimulation–providing the experimenters with a response rate as a measure of its pleasure-reward. The 0.5-second limit also guaranteed that the rats (or dolphins) would not stimulate themselves unto death: “The story is told of a dolphin who, inadvertently left in a pool with the switches connected, delighted himself to death after an all-night orgy of pleasure.”[45] [46] These precautions against “Death by Ecstasy,” as Larry Niven titled a fictional account of a murder, in which the “weapon” was a “pleasure plug,” accentuated the phantasmagoric image of the perpetuum.41

In attempting to place a value on self-stimulation and to incorporate EBS into existing scales, investigators matched it against hunger, thirst, sex, pain, fatigue, and more. Self-stimulation often prevailed over its competitors. It was “more than,” on the edge, off the grid, rather than in between the supposedly stable and coherent outliers against which it was matched. Animals preferred to starve to death rather than rationally calculate their pleasures and pains. These observations and modes of valuing EBS accentuated the extremity of the perpetuum by emphasizing its perverse pathological deviations from any notion of a rational felicity calculus.

The perpetuum was also a product of the unique relationships that were forged between the hypothalamus and human-induced artificial electrical stimulation of the brain. The perpetuum depended on the indefatigability of the hypothalamus, which received thousands of electrical stimulations and continued to react, unlike the motor cortex, which would enter a refractory period of unresponsiveness.

The investigators were partly cognizant of these–their own– constructions of the enacted phenomena. Some expressed the gap between an imagined pleasure and the pleasure that was necessarily constituted in laboratories. Any setup and measurement of pleasure construed pleasure and its measurement in particular ways. Trivial details, like the size of the lever and its relative size with respect to the overall size of the Skinner box partly determined the frequency of lever presses, as Olds observed.[47]

Lilly, who studied monkeys and dolphins, reported that in monkeys the rate depended on whether the monkey was required to press the lever with its hand (3 presses/sec- ond), tongue (2 presses/second), or foot (1 press/second).[48] Other investigators observed that when the stimulating electrodes were positioned in the substantia nigra the rat turned itself around after every lever press. As Roy Wise reminisced, “there was a pronounced motor effect, forcing the animal to turn 360° from and back to the lever between lever-presses. . . . St. Laurent, a post-doc of Olds made a movie of the different forms that self-stimulation could take.”[49] Still others reported that some rats stayed on the lever when given the opportunity to receive continuous brain stimulations, while others preferred short trains of electrical stimulations and turned off the current after a short burst. These and numerous other variations depended on the location of the stimulation and on the rat. These variations also prompted a variety of hypotheses. While some argued that rats self-limited their own EBS because prolonged stimulation became aversive, others explained that the rats were maximizing their pleasure. The latter group reasoned that, because the continuous stimulus might be habituating, the marginal returns–to rephrase the investigators– decreased over time. By getting on and off the lever, the rats increased their rewards.

There were also reports that could temper the dominant vision of the perpetuum. For example, in his observations of monkeys, Lilly noted that if “you make him [a monkey] push the lever with his tongue, he then reaches over and picks up a piece of apple with his mouth and stores it in the pouches on either side of his face, goes on pushing with his tongue and chews the food between pushes.”[50] Reports from human subjects and from dolphins described this resistance and refusal to press the lever if the experimenters made it too difficult or uncomfortable.[51]

In addition, self-stimulation was criticized as an absolute measure of pleasure- reward by prominent insiders, including Olds. The perpetuum provided more of an illusion or semblance of absolute quantification. Though many early publications implicitly vaunted the excess of numbers, Olds himself presented self-stimulation only as a comparative tool, objecting to its use as an absolute quantitative measure of reward-pleasure. This comparative perspective did away with any notion of absolute pleasure quantities. However, even this numerical compromise was criticized by some investigators, who established that self-stimulation did not correlate with other measures of reward. Most distinctly, when animals were given the choice to lever press and stimulate differently positioned electrodes in their brains, they often chose to press a lever that produced lower rates of lever pressing. This observation, however, was not indicative of the true measure of reward-pleasure, since, as some argued, the lower rates could simply indicate that the effects of the stimulation persisted for several seconds, rather than declining rapidly. Despite the criticisms, alternatives, and complications that haunted the perpetuum, the perpetuum largely overwhelmed its detractors both inside and outside the scientific community.


The image of an instantaneously produced, insatiable, self-perpetuating super-pleasure captured the imagination of contemporaries and of generations to come. Philosophers, legal scholars, psychologists, journalists, fiction writers, movie producers, and investigator- clinicians drew on the pleasured rat in challenging entrenched philosophical views (e.g., Gilbert Ryle’s language-based analysis of pleasure as a nonsensation);[52] in “query[ing] whether a constitutional issue, not to say a basic ethical issue, would arise if the offender’s submission to such ‘brave new-world’ wiring of his brain were made a legal condition for his being returned to society”;[53] in voicing concerns over governmental mind control and brainwashing; in seeking inspiration for artistic and cultural productions of a utopian or dystopian nature; and in suggesting new disease models and therapeutic interventions.

One major preoccupation was where to position the newly discovered super-pleasure in the social and natural orders. As Carol Tavris put it, “we hear of mysterious pleasure centers of the brain that turn the surliest male ecstatic when they are stimulated. Enthusiasts hail ESB [electrical stimulation of the brain] as a salvation for the sick and an antidote for the aggressive. Skeptics see visions of 1984: electrodes implanted in everyone, controlled by a computer that assures happiness and political docility.”[54] This quandary was relevant to Nature and humans alike. In terms of the natural order, investigators presented a nature that was both dependent on and wary of the new superpleasure. Previous naturalists and investigators had already incorporated (normal) pleasure into the natural history of animals or, after Darwin, into evolutionary theory. These latter incorporations presented a pre-Darwinian Nature, in which “the Creator has given to man the two faithful guards of pleasure and pain for his preservation; the one to avert evil, the other to invite him to useful actions,” as Albertus Haller put it in the eighteenth century; or, as the post-Darwinian perspective was summarized by Charles Scott Sherrington in the early twentieth century: “The concomitance between certain nervous reactions and psychosis seems an alliance that strengthens the . . . continuance of existence.”[55]

The post-Olds interpretations emphasized and took off from the super-pleasure. Pleasure was no longer just a motive or spring for action, but a positive feedback perpetuum loop that could disrupt even a minimal version of the felicity calculus of organisms. This image framed the animal kingdom in terms that were akin to human society. Both the animal kingdom and human society had to come to terms with their super-pleasure principle within a reality principle of the struggle for existence (animals) or the reality principle of society (humans). According to investigators, in the animal kingdom, the management of super-pleasure was built-in and wired into the hypothalamus of organisms and had to be so for the very possibility of their existence. They presented the following model: the architecture of the hypothalamus was made up of discrete centers of “pure” aversive-pain and “pure” reward-pleasure. These two principles interacted in the hypothalamus and were ultimately integrated into one output. These positive and negative centers–two for each drive–were in hyper-mode and were reciprocally interrelated and inhibitory.

At the atomic level of the hypothalamus, the brain was not a moderate consumer: its hunger or its pleasure or its sex was not construed on a model of moderation, but on extremes that were held in check and “released” when the conditions were appropriate. This basic model of “release” harked back to the nineteenth century, but the new model introduced significant distinctions. In the new hypothalamic model, the inhibiting centers were not exclusively “higher” centers that released “lower” centers. Investigators did not present a model of the “super-ego” that controlled the “id”–to transpose this new science into a different domain; an apt transposition, since various twentieth-century investigators explicitly positioned the id in the hypothalamus, both prior to and following the new discoveries.[56] The id was made up of drive-inhibit dyads, whose reciprocal and integrated interactions were the id. These inhibitors did not inhibit the id. They were part of the id itself. The higher centers indeed exerted control over the lower hypothalamus, as they had done before, but they were not the “stop” button in a model in which the lower id was exclusively “go.” They exerted their control over the go-stop dyad of the now dual/Janus-faced id, and they were demoted to ( just) one more type of input among several types of inputs into the hypothalamus, which now also included direct inputs from the internal environment of the body.

For human society, the implications of super-pleasure were more complex and knotty. Isaac Asimov, Abraham Maslow, Sandor Rado, John C. Lilly, Sidney Cohen, and several philosophers, each in his own way, presented the potential dangers of a society of pleasure or, rather, of a society of insatiable self-pleasuring individuals, of individualized pleasure gone mad. In this dystopia, the “invisible hand” collapsed from a pleasure that was way off the grid. The humanistic psychologist Maslow expressed this more general angst about super-pleasure in his comments on a 1955 presentation of the pleasured rat by James Olds, shortly after its initial 1954 discovery:

Supposing the subjective pleasure state brought on by septal stimulation turns out to be the end or goal of many kinds of motivated behavior… which has its goal, and therefore its justification, in a subjective, pleasurable, conscious state. Then what would happen if we could short-circuit or bypass the whole complex of troublesome . . . behaviors which have in the past been the only ways of achieving this pleasurable end-experience? . . . Would we eat? So for drinking, copulating, and temperature regulation? So also perhaps for love. … If complex civilizations are based upon forced, sometimes unpleasant work in order to get … a pleasurable subjective state, what would happen to work (and to civilization) if this same end could be achieved by plugging oneself into a nearby Olds-intermittent-stimulator-socket?[57]

Maslow had presented these apocalyptic visions of the super-pleasure in arguing for and insisting on an ethics of higher versus lower pleasures. The affirmation of distinct– higher versus lower–pleasures would safeguard against the breakdown of a civilization that had discovered the super-pleasure and made it technologically available. Similar concerns and analogous resolutions would appear in philosophical interrogations of the EBS. These philosophical commentaries, like “Pleasure Helmet and Super Pleasure Helmet,” ethicized and/or rationalized the new super-pleasure away by imagining and/ or construing and/or explicitly arguing for a hierarchy of lower versus higher motivations qua ethical and/or rational objectives in and meanings of life.[58]

Experimenters, however, had not discovered, nor had they proffered, an imagined “higher” pleasure in the brain. This higher pleasure would provide an easy and illusory solution for the predicaments of a society that came face-to-face with “supramaximal” pleasures, which were the source of all pleasures. Super-pleasure was, indeed, cerebrated, but it was distinctly non-“cerebral.” It was not a pleasure that assumed distinctions between a “low”-sensuous-embodied pleasure and a “high”-aesthetic-cerebral pleasure. These distinctions were established most significantly and pertinently in Kant’s work, when he differentiated between “rational, universal taste and appreciation” and “embodied, instinctual, voluptuous stimulation.”[59] Cerebrated (noncerebral) pleasure presented a model of the brain in which the “higher”–neocortical–“cere- bral” pleasures had their source in the cerebrally “low” subcortical brain centers or circuits of pleasure. This topology of the brain also ensued from earlier observations during the 1940s and early 1950s, in which experimenters discovered that the neocortex was devoid of pleasure neurons and that its direct stimulation did not yield pleasure (in humans). All pleasures were low pleasures. These discoveries implicitly democratized pleasure by leveling all pleasures. They also undermined ideologies and cultures that were invested in these distinctions.[60] This implicit challenge from the laboratory resonated, but it did not seem to reverberate, with significant analogous and contemporaneous shifts in pleasure beyond the laboratory.

These particular concerns with higher and lower pleasures, ethics, meanings, and objectives were largely absent from much of the vernacular literature. It was not the frenzied hedonism of these rats, their unbridled self-stimulation, and their disruption of a rational and calculating self that evoked widespread concerns. It was the specter of mind control. Midcentury commentators were captivated by the Cold War era literature on “mind control” and “brainwashing,” including Hidden Persuaders (1957).[61] Several investigators further accentuated these vernacular concerns, notably Jose M. R. Delgado. Delgado, who was one of the pioneers and a well-respected researcher from

Yale at the time, performed various controversial demonstrations of brain control in bulls and monkeys, which led to the publication of his widely read monograph, Physical Control of the Mind, in 1969.[62]

These widespread public concerns with direct mind control by despotic overseers, however, failed to internalize the true meaning of the super-pleasure. Invoking Al- dous Huxley, Lilly perspicaciously observed of the new technologies, “The Brave New World will not be imposed upon us by Big Brother. We will beg for the raptures of Soma and call it a sacrament.”[63] Skinner would make a similar astute observation in the course of his testimony during the 1973 Kennedy hearings on human experimentation: “Punishment has at least the merit that it generates countercontrol. The punitive controller eventually runs into trouble, but the positive controller may achieve a new and frightening kind of despotism.”[64]

Yet even these two astute observers seem to have underappreciated the full meaning of the perpetuum. Several post-“Olds-intermittent-stimulator-socket” authors– as Maslow referred to Olds’s new technology–seem to have grasped and internalized the meaningful distinctions between the new EBS “super-pleasure” and Huxley’s obsolete model of “Soma,” which was often invoked as prescient in the brain-control literature.

Larry Niven’s fictional account of “Death by Ecstasy” (1969) exemplifies this new work. Niven drew on the new super-pleasure in constructing a crime scene in which the deceased, “Owen,” died from an “ecstasy plug” that was wired into his “pleasure center.” Death ensued from starvation and “lack of will power.” As one of the protagonists explained, Owen died after a “month of ecstasy, a month of the highest physical pleasure man can attain . . . [though] food [was] only a few footsteps away,” Owen would “have [had] to pull out the droud [electronic brain implant] to reach it.”[65]

“Soma,” Huxley’s drug of blissful happiness, projected an image of a pleasure of contentment and conformity, of incorporating the dominant ideology of a society and the order of things–of a productive pleasure, in terms of the totalitarian regime of the Brave New World. Soma was overtly functional for the Brave New World, rather than disruptive of the social order. The new super-pleasure was not a pleasure of comfort and acquiescence, nor of docility, nor of acceptance. It was a super-pleasure that overwhelmed; it disrupted production and the reproduction of obedient subjects and society. It was a pleasure that killed. These distinctions between Huxley’s food pellet, ingested Soma, and the new direct brain-stimulated super-pleasure are perhaps best captured by and/or are analogues to the suggestive distinctions between plaisir-pleasure and jouissance that emerged in Lacanian theorizing during the same historical moment.[66] Moreover, these distinctions, as I will argue below, also capture and reflect the shift from an older social order, which was embodied in a lever-pressing rat that was rewarded by a food pellet, to the new social order, which was embodied in a lever-pressing rat that was rewarded by direct brain stimulation.


In the Lacanian concept of jouissance, and in current scholarship on pleasure, much attention is focused on sex and the erotic body–“How difficult it is to uncouple the terms pleasure and sexuality,” Cora Kaplan rightfully observed. For mid-twentieth- century investigators, however, there was much more to pleasure than sex (or drugs).[68] During the initial phase of the science of pleasure, sex and the erotic writ large were conspicuously absent.[69] The brain science of pleasure was initially and predominantly a study of hunger pleasure-reward, and less so of thirst pleasure-reward. Sex pleasure- reward appeared soon after. Thermoregulation pleasure-reward, aggression pleasure- reward, and drug pleasure-reward would also join the fray.

These distinctions between drive-specific rewards-pleasures emerged from the very beginning of the new discoveries. Investigators discovered a gamut of drive-specific rewards-pleasures, one for each drive: a feeding-drive reward-pleasure, a sex-drive reward-pleasure, a thirst-drive reward-pleasure, and so forth. Each drive-specific reward- pleasure was independent of the others, was semidistinct anatomically, and was sensitive to different experimental manipulations.

The iconic, self-stimulating, insatiable super-pleasured rat that was invoked in numerous publications and images was more often than not stimulating its feeding- center pleasure site (or its drinking-center pleasure site), and not its sex-center pleasure site or its orgasm pleasure site. In terms of laboratory enactments, there was nothing unique about sex pleasure/reward. Its mode of production, measurement, and reward/pleasure value were indistinguishable from other pleasures-rewards. There was no distinction between the stimulation of the pleasure-reward zones of the thirst drive, the feeding drive, the thermoregulation drive, or the sex drive. The self-stimulating rat was also indifferent to these distinctions, and during the protocol, the experimenters were often ignorant of and indifferent to the drive specificity of the “reward” electrode prior to the dissection of the rat’s brain.[70]

The innumerable allusions to and depictions of the insatiable ecstatic rats as inspirations for varieties of orgasm-inducing–“Orgasmatron”-like–brain machines ought to have been framed and named in terms of “drinkotrons” (thirst-drive super-pleasure) or “feedotrons” (feeding-drive super-pleasure) or even “thermotrons” (thermoregulation- drive super-pleasure). These names would have more realistically reflected the true nature of these early devices. The pleasure-frenzied rat was not experiencing a barrage of orgasms, but a barrage of feeding super-pleasures, drinking super-pleasures, and so forth. In fact, and as experimenters clearly showed, when given the choice between the stimulation of their thirst-center reward-pleasure site by EBS and real sex with a real female in heat, male rats preferred the thirst-drive super-pleasure over copulation.

These varieties of nonsexual super-pleasures presented a gamut of polymorphous pleasures. But these polymorphous possibilities were lost on contemporaries and on the cultural imagination of future generations. They represent “missed” pleasures and missed paradigms and templates for and of pleasure.72 Super-pleasures were orgasms, which were now streamlined. The orgasm usurped super-pleasure and framed for many the 1960s pleasure revolution–and for some, women’s liberation–in terms of a sexual-pleasure revolution.73 The orgasm hijacked (and high jacked) the perpetuum.14

Scientists were also partly hijacked by the orgasm conception, despite their enactments of polymorphous pleasures. Some, like Lilly and Cohen, explicitly referred to the frenzied rats (monkeys and dolphins) in terms of orgasms, despite knowing better. For others, the basic stipulations of the laboratory and of scientific protocols partly prescribed the orgasm as an implicit model for studying pleasure. Instantly reproducible, rapidly climaxing, and immediately dissipating–the orgasm template offered a discrete moment-phenomenon, which was clearly distinguishable from background fluctuations, could serve as a focal point for research, and could be conditioned, in contrast to the hunger-satiety template, which was spread over time, was not a moment in time, and progressively and insidiously metamorphosed from hunger into satiation, with no clear demarcations between its presence and absence.

The requirement for instantaneity in reward studies was ostensibly presented by Neal E. Miller, for whom EBS was a godsend, since it allowed him to produce instants: instant hunger, instant satiety, and instant thirst. EBS transformed hunger, satiety, and thirst–which were intractable–into phenomena that were instantaneous and brisk. Miller redesigned hunger, thirst, and satiety in these terms, since his conditioning experiments demanded a definite and brisk change in the animal economy.15 EBS bypassed the temporal order and logic of the body and its materialized-embodied reverberations. It redesigned super-pleasure in terms of the momentary, climaxing, and fleeting orgasm moment. The science of pleasure-reward thus offered polymorphous pleasures, but it also implicitly designed them on an orgasm template.

The orgasm template was also partly prescribed by the English language. There seems to be no specific word in English for a “supreme pleasure moment” of eating- satiation or drinking-quenching. There seems to be no analogue to orgasm in speaking of a gastronomic experience (other than the derived and contemporary collo- quialism–“foodgasm”). The seeming absence of a way to speak (and think) about extreme pleasure moments of biological drives other than in terms of sex positioned orgasm as the only available template for imagining and speaking these moments.

12      For an exemplary account of an alternative, pre- and non-sex-dominated conception of pleasure during the Enlightenment, see Emma Spary, Eating the Enlightenment: Food and the Sciences in Paris, 1670-1760 (Chicago, 2012), esp. chap. 5.

13       On the association between women’s sexual-pleasure revolution and women’s liberation, see, famously, Anne Koedt, “The Myth of the Vaginal Orgasm,” in Notes from the Second Year (New York, 1910), 31-41. See also Jane Gerhard, “Revisiting ‘The Myth of the Vaginal Orgasm’: The Female Orgasm in American Sexual Thought and Second Wave Feminism,” Fsmin£LSy&— 26 (2000): 449-16.

14        I thank Robert Gregory Boddice for introducing me to the meaning of “high jack.”

15      E.g., according to the drive-reduction theory, the instantaneous production of satiety via EBS should work like a reward.

There were, nevertheless, other contemporaneous models for imagining and framing extreme pleasures: drugs (LSD and narcotics) and nirvana. Rado, Lilly and Cohen, and the vernacular literatures proffered these other possibilities. In respect to drugs, the associations with the perpetuum were already evident by the early 1960s. These drug associations were for the most part absent from the publications of the broader community of expert ESB reward investigators. The associations between EBS reward and drugs were of two kinds. For Rado and for Lilly and Cohen, the major thrust of the links was in terms of shared hyper-pleasure. Drugs and the perpetuum were instances of “supramaximal” pleasure (Lilly, in speaking of LSD) or “superpleasure” (Rado, in speaking of narcotic drugs and addiction–“bondage”). The link with EBS was in terms of the unique and shared experience of excessive pleasure (which for Rado also explained the addiction). This link via excessive pleasure, and the modeling of addiction in terms of an addiction to pleasure, explains why the broader community of EBS experimenters ignored both of these possible connections. Many EBS investigators did not speak (or think) in terms of pleasure. The EBS rats, moreover, were not “addicted” to the EBS, at least not in terms of the physiological meaning of addiction, which framed addiction primarily in terms of withdrawal, rather than in terms of being addicted to the “pleasure” of drugs.[71] In the vernacular literature, the preoccupation with mind control forged immediate associations between EBS and drugs. Both represented different methods for brain control: electrical and chemical, respectively.[72]

The nirvana model potentially offered a real alternative to the EBS-orgasm model. As Lilly explained in retrospect, the science of the orgasm and the template of the fleeting climaxing moment were incompatible with nirvana, which was an extended and sustained pleasure state. EBS-orgasm failed as a model for this different superpleasure possibility and cosmology. For Lilly, moreover, nirvana could be achieved by extremes of pain, rather than only in terms of pleasures.[73]

For Maslow, in contrast, the relationships between the perpetuum and nirvana, or rather, between the perpetuum and “mystic or oceanic experiences,” were not oppositional, as they were for Lilly. Rather than focusing on the pleasure of super-pleasure, addiction, or alternative cosmologies of nirvanic–nonorgasmic–pleasures, Maslow emphasized that the rats were oblivious to the outside world–to the external environment– during lever pressing. This withdrawal into the self, which could model various pathologies, like schizophrenia, was also typical of “beatific states of concentration on ‘higher’ conscious experiences reported from the East, as well as with the concentrated fascination of aesthetic and cognitive insight experiences.”[74] The perpetuum was turned on its head. Rather than modeling a frenzied pleasure and its dystopic possibilities, as Maslow had done several paragraphs above in this same commentary, he presented the frenzied rats as existing on or modeling higher states of consciousness–as, in fact, modeling nirvana.


There was one other possibility for why the orgasm was more appealing than nirvana in modeling super-pleasure. This possibility was not articulated explicitly, but it emerged from an interchange between Lilly and Cohen, in which they discussed, among other things, what a society of nirvana would have to look like. If the nirvana model of EBS were to function as a general model for Western society, if Western societies were to adopt EBS-nirvana as a common practice (rather than EBS-orgasm), then it would require the imagining of a different social organization. This social organization was imagined to exist in the East by Lilly and Cohen, and to be incompatible with the Western social order. The Western model of democratized access to superpleasure and ecstasy could not tolerate, afford, or support a nirvana model, a model of instantly produced extended nirvanas, in which a large segment of the population would enter and sojourn in prolonged states of nirvana-induced EBS. The EBS-as- nirvana society was thus at odds with the cultural imagination and possibilities of Western EBS investigators and their vernacular audiences. The EBS-orgasm model, on the other hand, was instantly appealing. It was instantly produced, immediately climaxed, and it dissipated instantaneously. It could easily be incorporated and integrated into, and managed within, Western society, and it was easily imagined by Western minds in terms of their society.

It was also good for business. This latter “good” of the EBS-orgasm brings us back to one unresolved issue in respect to the perpetuum, which links several threads of this history together. Considering all the negative press of super-pleasure, why did Nature select for a super-pleasure that continuously positioned organisms on the edge of their own perpetuum? A full discussion of this significant question is beyond the scope of this essay. Below, I briefly outline in broad strokes one interpretation that took shape during this initial period.[75]

Throughout the period under study, EBS-rewarded rats and the perpetuum were often under suspicion. The preternatural presentation and materialization of EBS continuously undermined its status as a model of nature.[76] The naturalization of EBS entailed crucial and fascinating developments and experiments in a broader postwar cultural context that was itself rapidly shifting. In the context of this broader transformation, one discovery encapsulates the significance of the shift to super-pleasure, the evolutionary logic of the perpetuum, and the emerging postwar consumer market. This discovery was the perplexing finding that stimulation of the hunger center was rewarding. Experimenters observed that the same electrical stimulation that was rewarding for the rat also activated the rat’s hunger drive. Why would a rat frantically press a lever that made it hungry, and why was it rewarding for the rat?

This discovery was inexplicable in terms of the drive-reduction theory, in which hunger was an aversive state of deprivation that activated the animal into a state of high drive. The driven animal found food, ate, and was satiated. Satiety, not hunger, was thus rewarding (pleasure), since it reduced the hunger (drive). In evolutionary terms and as Miller succinctly put it: “Animals who are not pleasantly rewarded by substances that reduce their drives come from a long line of extinct ancestors.”[77] This basic scheme of the drive-reduction theory also implied an economy of scarcity: it was enacted inside the laboratory by depriving animals prior to the experiment and provisioning food, sex, water, and more as the “reward” during the experiment. This implied scarcity economy, its enactment inside the laboratory, and its affective logic of an aversive hunger and a rewarding satiety were turned upside down with the discovery of super-pleasure in the brain. The new super-pleasure-in-the-brain cerebrated and embodied an economy of affluence and of pleasure seeking: of consumption in satiety– of consumption that was driven not by deprivation, but in satiation and within an economy of abundance, since EBS-rewarded rats were satiated; and of an insatiable “hunger” that was, moreover, rewarding, rather than aversive(!). This was the enacted discovery of the new super-pleasure: a satiated, nondeprived rat that continued to press the lever insatiably and was continuously “hungry” for more re- ward–for, in fact, more “hunger.” “Eating begets eating,” as Olds succinctly put it.[78] This was the meaning of the perpetuum in its real embodied and natural form, that is, in terms of the drives to which it appertained (since all rewards and pleasures appertained to drives and were never abstract).

In trying to make sense of these discoveries, Olds proposed a new hypothetical and tentative model of the relationships between hunger, satiety, and starvation, which could be broadened to all other drives, and in which he accounted for the EBS- rewarded behavior, evolutionary theory, and the perplexing (for the older model) finding that hunger was rewarding.[79] First, he analogized between the albino rat–“having been bred in a laboratory”–and the average American college student–“having been bred in America”–neither of which “has ever experienced a need in its life.” What, then, he wondered, “might drive behavior in the absence of needs”? The drive- reduction theory, he continued, was a “Procrustean bed” for “an organism that seeks novelty, ideas, excitement, and good-tasting foods.” He then surveyed some of the major scientific findings since his initial discovery, and then he turned to consumption. He emphasized the positive feedback loop of consumption–“Once the eating mechanism has been triggered, it moves forward under its own power and would go on indefinitely if other extraneous control devices were not brought to bear.” But “why does the animal keep on eating?… Why does the animal start eating even if he is not starving, but is only stimulated by the sight or smell or taste of food?”

Evolution made sense of these seemingly inexplicable behaviors:

[the] mechanisms for hoarding promoted the survival of the species. The abstract animal (who never lived so far as I can make out in phylogenetic history) who waited until demise was imminent and then began looking to satisfy his need was on the edge of demise at all times. You might say he was “just” living. His lucky cousin, who is no abstraction, stocked up his larder during the fat years, in preparation for the lean ones, and you might say he enjoyed it. Instead of “just” living, the positive reinforcement creature was really living.[80]

The relationships between consumption, affect, and drive had shifted from an economy of (wartime) scarcity and food rationing and from an experimental program that took off from deprivation and “drive reduction” to a (postwar) political and experimental economy of abundance and consumption, in which satiated humans were driven insatiably to consume, and in which satiated animals inside laboratories were driven insatiably to self-stimulate their brain pleasure circuits.[81]


Roy Wise still remembers the fascination with and the gravitational pull of the per- petuum during his graduate studies in the 1960s, walking down the hall and hearing the noise of the clicking of relays of electrical stimulation, and the abundant “pleasure”- talk, in which he, in his youth, was also caught up during one instance.[83]

There was (and still is) something irresistible about the lever-pressing, selfstimulating, insatiable rat. The pleasure revolution of the mid-twentieth century was a revolution by revolutions–a simple rattine lever press repeated hundreds of thousands of times. Perhaps it was only as a perpetuum that pleasure could be heard in the context of the behaviorism from and in which it initially emerged. Would there have been “pleasure” if it were not for the perpetuum, if it had emerged in terms of mazerunning or electric-grid-crossing rats? The repetition of these repetitions in a growing number of laboratories was at the heart of the scientific revolution in pleasure. The be- haviorist’s toolbox of repetitions and frequencies of repetitions materialized “pleasure” and made it supramaximal.[84]

As supramaximal, as a perpetuum, pleasure was perhaps too “super” for a postwar society that wanted its super-pleasures but still retained a powerful notion of selfmastery and of “healthy” hygienic pleasure. As Maslow said of “peak experiences” (which he had on previous occasions explicitly compared to the perpetuum rats), “They would kill us if they lasted too long or came too often. (Supposing a great orgasm lasted for 15 minutes instead of 10 or 15 seconds! The organism couldn’t stand it. Surely the heart would collapse.)”[85] In the mid-twentieth-century United States, rats, monkeys, dolphins, and (institutionalized) patients were the sole beneficiaries– or subjugated victims–it seems, of supramaximal, super, pure pleasure.[86]

The endlessly repetitive, mechanical, and factory-like lever presses of the hardworking rat were neither alienating, nor tedious, nor boring for the rat.[87] Tedium, boredom, habituation–these ostensible effects of repetition were absent from the literature on repetitions in lab rats and in lab “hermits,” as G. Stanley Hall christened the new breed of late nineteenth-century laboratory-based researchers. These hermits were the human version and equivalent of lab rats.[88] They were looped in a per- petuum of their own: the perpetuum of knowledge. They engaged in endless repetitions and replications (though they were beaten by the rats), had an insatiable appetite (for knowledge), were indefatigable, and like the rats, they renounced food, sleep, sex, and sensual gratifications (for the sake of knowledge)–for the “reward,” perhaps even (super) pleasure, of science.[89]

This parallelism between rats and scientists can be taken one step further. Like a lab rat that accidentally and serendipitously pushed the lever of pleasure-reward and went into a frenzy of repetitions, the science of pleasure-reward writ large was a science that literally began with–and was often described in terms of–accidental serendipitous discoveries, which were followed by a frenzy of repetitions and replica- tions.[90] This core narrative and formula, in which the effect of an accidental and contingent behavior of an organism leads to an exponential increase in the frequency of repetitions of the (accidental) act that had preceded the effect, constituted the primary and basic definition of the behaviorist-Skinnerian “positive reinforcement” and “reward.”



John Liggins, B.Sc. Department of Psychiatry McGill University, Montreal June 2011

A thesis submitted to McGill University in partial fulfillment of the requirements of the degree of Master of Science in Psychiatry.

© John Liggins, 2011



Without the help and support of so many incredible individuals, a project of this magnitude would not have been possible. I would like to thank the following people: Dr. Marco Leyton, my research supervisor, for the opportunity to conduct this study and for the superb assistance, guidance and mentoring he has provided me with over the past four years. Dr. Robert Pihl, my co-supervisor, for setting me up with the current project as well as for the countless and extremely helpful theoretical and philosophical discussions we have had over the years. The people in my lab — Kevin, Vinod, Elaine, Krzysztof and Elizabeth — who helped to steer me in the right direction, provided excellent advice and technical assistance and shared the same day-to-day experience of research and graduate school. Kathleen Auclair, the research nurse associated with the study, for her patience and excellent service. The other collaborators on the project — Ava-Ann Allmann and Dr. Chawki Benkelfat — for theoretical discussions and some technical assistance.

The work that I have completed over the past four years would not have been possible without the support, advice and encouragement so generously provided to me by my family and friends. I am deeply indebted to Mitch, Patrick, Niels and my father for their unfailing support, through good times and bad times, as well as all of the fun times we have all had together.

I helped design the study and I executed all aspects of the experiment. I wrote the first draft of the manuscript contained within this thesis. At the time of submission, only Drs. Marco Leyton and Robert Pihl have seen this draft.



A large body of evidence indicates that dopamine (DA) neurotransmission regulates approach toward rewards and reward-related cues. The best-cited hypothesis proposes that DA accomplishes this by mediating the pleasurable effects of a variety of natural and drug rewards. This “anhedonia hypothesis” has received support from some pre-clinical models of reward and a few drug challenge studies in humans. However, direct assessment of DA’s role in mood and other subjective states in healthy humans has been largely limited to the use of psychostimulant drugs, which elevate brain levels of multiple neurotransmitters in addition to DA. This thesis is comprised of one study which examined the effect of more selectively elevated DA neurotransmission, as produced by administration of the immediate DA precursor, L-DOPA, in healthy human volunteers. L-DOPA failed to alter mood and other subjective states. These results add to the evidence that DA neurotransmission does not directly influence mood in healthy humans.



La contribution precise de recompense et de motivation de la neurotransmission de la dopamine (DA) n’est pas entierement comprise. La meilleure hypothese citee propose que la DA forme un trait d’union des effets agreables d’une variete de recompenses naturelles et narcotiques. Cette hypothese « anhedoniste » a requ l’appui de quelques modeles precliniques de recompense et de quelques etudes chez l’humain mettant la drogue en question. Cependant, revaluation directe du role de la DA sur la disposition et autres etats subjectifs chez l’humain en sante a ete principalement limitee a l’utilisation de drogues psychostimulantes, ce qui eleve le niveau de neurotransmetteurs multiples en plus de la DA dans le cerveau. La presente these comprend une etude qui examine l’effet d’une neurotransmission selectivement plus elevee de la DA, produite par l’administration du precurseur immediat de la DA, L-DOPA, chez des volontaires en sante. L-DOPA n’a modifie ni disposition ni autres etats subjectifs. Ces resultats s’ajoutent a l’evidence la neurotransmission de DA n’influence pas directement la disposition chez l’humain en sante.



1.0  Dopamine biochemistry

Dopamine (DA), norepinephrine (NE) and epinephrine are collectively referred to as catecholamines due to the presence of a common catechol or hydroxylated aromatic ring nucleus in each of the molecules. Catecholamines function as neurotransmitters in the central nervous system and they are also biologically active in a variety of peripheral body tissues. DA, for example, is found primarily in the brain, but also to some extent in the kidneys (Missale et al 1998). Catecholamines share a common biosynthetic pathway, beginning with the essential amino acid phenylalanine (Kuhar et al 2006). Within the liver, phenylalanine is a substrate for phenylalanine hydroxylase (PH). PH adds an hydroxyl group to produce tyrosine. In catecholamine neurons, tyrosine is a substrate for the rate-limiting enzyme in DA synthesis, tyrosine hydroxylase (TH). The addition of the second hydroxl group produces dihydroxyphenylalanine (L-DOPA). L-DOPA, in turn, is a substrate for DOPA decarboxylase, which rapidly converts the precursor into DA. In neurons that release DA, this is the terminal step in catecholamine synthesis. The majority of DA neurons are found in two adjacent and somewhat overlapping brainstem nuclei, the ventral tegmental area (VTA) and the substantia nigra (SN; Kuhar et al 2006). DA neurons from the former area project to a variety of cortical and sub-cortical regions, including the prefrontal cortex, amygdala and ventral striatum (VS), while DA neurons from the latter structure project mainly to the dorsal striatum (Kuhar et al 2006). In other brainstem neurons, catecholamine synthesis does not stop with the formation of DA. Some of these neurons possess the enzyme DA P-hydroxylase (DBH), which converts DA into NE, while a minority of others also possess the enzyme phenylethanolamine N-methyltransferase, which converts NE into epinephrine (Kuhar et al 2006). Catecholamine synthesis in the periphery involves the same enzymes.

Of particular relevance to the present discussion are the storage, release and post-synaptic signalling features of the DA system. DA is most commonly synthesized in the pre-synaptic terminal of DA neurons, though synthesis also occurs in the cell body. Following DA synthesis in the cytosol, the neurotransmitter is actively transported into vesicles via the vesicular monoamine transporter (VMAT). DA release can be “phasic” which occurs in response to increases in the firing rate of DA neurons or “tonic” which is not activity- dependent and contributes to the basal level of DA present in synaptic and extrasynaptic areas (Grace et al 2007). Synaptic DA levels are generally regulated by pre-synaptic DA release and post-release clearance mechanisms. The latter involves reuptake of DA into the pre-synaptic terminal by the DA transporter (DAT) and ultimately its degradation into inactive metabolites by the enzyme monoamine oxidase (MAO). In most brain regions, DA can also be metabolized in an extraneuronal fashion by the enzyme catechol-O-methyltransferase (COMT) which is present in the synaptic cleft. Clearance by COMT is the dominant mechanism in the prefrontal cortex and clearance by DAT is the dominant mechanism in the striatum (Matsumoto et al 2003). DA exerts its post-synaptic effects by binding to one of the five different DA receptor subtypes (Missale et al 1998). These are divided into two major families, the D1-like (D1 and D5) and D2-like receptors (D2, D3 and D4). All of the DA receptors are metabotropic receptors that signal through the creation of second messenger molecules, such as cAMP, which influence a variety of chemical cascades that in turn affect downstream targets such as gene transcription and receptor activity. DA receptors can be found pre-synaptically where they function as autoreceptors that regulate DA release or post-synaptically where they convey molecular signals to other neurons (Kuhar et al 2006).

2.0  Dopamine, reward and the anhedonia hypothesis

A series of groundbreaking studies conducted in the 1950s with electrical brain stimulation (EBS) served as a critical catalyst for investigations into the neurobiology of reward and motivation. This approach was combined with a new operant conditioning paradigm to explore the potential involvement of cortical and sub-cortical structures in reward and punishment. Skinner’s behavioural theory of reinforcement (Skinner 1938) allowed for the objective measurement of behavioural responses related to reward and punishment. Briefly, a reinforcer was defined as any stimulus that served to increase the probability and frequency of actions that preceded its presentation (Skinner 1938). Thus, the frequency with which an animal responded by pressing a lever in a box, called instrumental responding, could be taken as a measure of the “rewarding effects” of a stimulus presented to that animal. In a landmark study, Olds and Milner (1954) combined EBS and operant conditioning and found that rats responded more frequently and vigorously on the operant lever in order to self-stimulate a variety of cortical and sub-cortical regions, including the lateral hypothalamus, cingulate cortex and brainstem. In stark contrast, though, rats did not increase their level of responding in order to receive EBS in other areas of the brain, including motor and sensory cortex. These and other observations made it clear that the brain contains specific anatomical substrates and circuits that correspond to basic biological drives, including sex, drinking and feeding (Coons et al 1965; Glickman & Schiff 1967; Olds 1956; Olds & Milner 1954).

Work over the next decade led to the suggestion that a specific neurotransmitter mediated reward processing in the brain. Evidence for this proposition came from anatomical and pharmacological studies involving the EBS self-administration paradigm. First, the mechanism by which EBS of the median forebrain bundle enhanced instrumental self-administration behaviour in rats appeared to involve stimulation of noradrenergic fibers of passage (Dresse 1966) and the consequent release of NE from these nerve terminals (Stein & Wise 1969). Second, drugs that altered NE neurotransmission produced dramatic changes in EBS self-administration behaviour. Specifically, drugs that augmented NE neurotransmission, such as amphetamine and MAO inhibitors, increased instrumental responding for EBS (Poschel 1969; Stein 1964), while drugs that attenuated NE neurotransmission, such as DpH inhibitors, reserpine and alpha methylparatyrosine (AMPT), decreased instrumental responding for EBS (Gibson et al 1970; Wise & Stein 1969). These and other observations formed the foundation of the NE hypothesis of reward (Poschel & Ninteman 1963; Stein 1964).

Around the same time, DA was gaining attention as a potential neurotransmitter. Although DA was initially believed to function only as a precursor for NE synthesis, this view started to change when Arvid Carlsson and colleagues (1957) found that L-DOPA restored motor activity in reserpine-treated rabbits. While this study left open the possibility that L-DOPA produced its effect by elevating NE rather than DA levels, two subsequent studies provided strong evidence that DA was in fact the critical mediator. Tissue culture experiments revealed that L-DOPA more potently elevates DA levels compared to NE levels in the brain (Carlsson et al 1958) and that these neurotransmitters are synthesized in discrete, non-overlapping brain regions (Carlsson et al 1957). Since the latter study demonstrated that DA is synthesized to a high degree in the striatum and this brain region was known to be an important substrate for motor function, it was proposed that DA neurotransmission plays a key role in motor activity. The efficacy of L-DOPA as a treatment for the motor symptoms in Parkinson’s disease (PD) strengthened this notion further.

Following the general acceptance of DA as a neurotransmitter, critical evidence emerged suggesting that it too was involved in reward. DA was first implicated in reward function based on the observation that electrode placement in brainstem nuclei that contained the cell bodies of DA neurons was sufficient to generate robust self-administration of EBS in rats (Crow 1972a; Crow 1972b; German & Bowden 1974). Next came the observation that systemic amphetamine administration enhanced instrumental responding for EBS when electrodes were placed in one of the loci of DA neurotransmission, the SN, as well as in the hypothalamus, which was believed to contain mainly noradrenergic fibers of passage (Phillips & Fibiger 1973). A role for DA in this behavioural phenomenon was suspected since both isomers of amphetamine were equally effective at increasing instrumental behaviour for EBS despite the fact that d-amphetamine exerted more potent effects on NET compared to l-amphetamine. These two major findings from the EBS studies prompted the creation of a broader catecholamine hypothesis of reward, which posited that both DA and NE were important neurotransmitters for reward function.

Investigators then conducted carefully controlled anatomical and pharmacological studies over the next decade in pursuit of confirmatory evidence for this new hypothesis. Surprisingly, though, a role for NE in mediating the rewarding effects of EBS was not supported by most of the evidence. Drugs that attenuated NE neurotransmission appeared to disrupt instrumental responding for EBS by altering arousal rather than reward function (Fouriezos et al 1978; Franklin 1978; Roll 1970). For example, in the study by Roll (1970), the DpH inhibitor disulfiram dramatically altered arousal as evidenced by the observation that rats fell asleep during brief pauses between EBS self-administration sessions. The key finding from this study was that disulfiram-treated rats resumed normal levels of instrumental responding for EBS when awoken by handling and placed back in front of the lever, suggesting that the rewarding efficacy of EBS remained the same, but that the lower levels of instrumental responding previously reported (Wise & Stein 1969) were due to the sedative effects of the drug. Furthermore, specific lesions to the NE fibers of the dorsal component of the median forebrain bundle failed to disrupt instrumental responding for EBS when the electrode was placed in either the locus coeruleus, a major locus of NE cell bodies in the brainstem, or the lateral hypothalamus, a structure densely innervated by NE fibers (Corbett et al 1977). A subsequent anatomical study determined that the cell bodies of NE neurons in the locus coeruleus did not overlap with the locations of electrodes in this region of the brainstem that supported self-administration of EBS (Corbett & Wise 1979). Since EBS did not appear to depend on activation of NE neurotransmission to generate rewarding effects, the role of this neurotransmitter in reward function started to come into question.

In contrast, similar experimental approaches provided some support for the idea that DA neurotransmission was an important part of the mechanism by which EBS produced its rewarding effects, though this was not without controversy. A series of drug challenge studies demonstrated that DA receptor antagonists strongly disrupted performance in EBS paradigms (Fibiger et al 1976; Franklin 1978; Franklin & McCoy 1979; Gallistel & Karras 1984; Rolls et al 1974; Wauquier et al 1972; Zarevics et al 1977). Initially, this performance deficit was attributed to an effect of DA receptor antagonists on motor activity rather than reward function (Fibiger 1978; Fibiger et al 1976; Rolls et al 1974). For example, in the study by Fibiger et al (1976), the DA receptor antagonists haloperidol and pimozide both significantly reduced instrumental responding for EBS of the lateral hypothalamus. Since the number of lever presses dropped following drug administration and remained depressed throughout the test session, the authors concluded that the performance deficit was due to an effect of the drugs on motor activity. If the DA receptor antagonists disrupted performance because of an effect on reward function, the authors reasoned, an extinction curve characterized by an initial increase, followed by a progressive decrease, in instrumental responding should have been observed.

Subsequent studies that were specifically designed to tease apart the effect of DA receptor antagonists on motor activity and reward function provided crucial evidence to suggest that these drugs were in fact altering reward function while leaving the capacity to respond intact. A notable series of experiments by Fouriezos et al (1978) provided compelling evidence. In the first experiment, the DA receptor antagonists pimozide and butaclomol both significantly and gradually decreased the instrumental response rate for EBS of the lateral hypothalamus. The resemblance of the pattern of drug effects to the extinction effect produced by reducing the current intensity of EBS implied that DA receptor antagonists reduced the rewarding effects of EBS in a similar manner. Indeed, the parallel between the effects of drugs and non-reward on instrumental responding is very important when interpreting the results of self-administration studies, since it is assumed that the animal gradually ceases to respond for a reward while under the influence of a drug because it comes to experience that reward in the same way that it experiences non-reward. In the second experiment, Fouriezos et al (1978) observed that pimozide-treated rats initially responded at higher rates when they came back into contact with the lever after a brief timeout period that followed the initial extinction phase, though no EBS was available. The high levels of responding suggested that the pimozide-induced performance decrement in the previous experiment was not due to a drug-induced motor effect. In the third experiment, Fouriezos et al (1978) used a different self-administration paradigm to extract specific measures of motor and reward performance. In this paradigm, rats had to run down a long alley in order to press a lever and receive EBS. Running latency provided a measure of the ability to initiate a motor sequence, while running speed and self-stimulation rate provided measures of the ability to execute complex motor sequences. At the beginning of the extinction trials, pimozide-treated rats had normal running latencies, running speeds and self-stimulation rates when compared to vehicle-treated controls. However, as the session progressed, running latencies increased and both running speeds and selfstimulation rates decreased significantly compared to controls. These results suggested that pimozide-treated rats decrease self-administration of EBS due to an effect of pimozide on the rewarding efficacy of EBS and not because of a drug- induced inability to initiate and execute motor responses.

The high rates of instrumental responding required in EBS selfadministration studies are a major limitation in reward studies, since even minor drug effects on motor performance can result in severe performance impairments. Consequently, an approach called the reward summation function was developed in an effort to reduce the impact of high response rate requirements and enhance the ability to detect the effect of experimental manipulations on reward function (Edmonds & Gallistel 1974; Edmonds & Gallistel 1977; Edmonds et al 1974). Using this approach, pimozide was shown to dramatically reduce the rewarding effects of EBS as evidenced by a shift to the right of the reward summation curve (Franklin 1978; Franklin & McCoy 1979; Gallistel & Karras 1984), providing further evidence that DA receptor antagonists disrupt instrumental responding for EBS by impacting reward function rather than motor activity. Further pharmacological support for the proposition that DA was involved in EBS came from observations that DA augmenting drugs enhanced the rewarding efficacy of EBS as evidenced by dramatic increases in instrumental response rates or responding to lower current thresholds (Crow 1970; Gallistel & Karras 1984; German & Bowden 1974; Phillips & Fibiger 1973; Poschel & Ninteman 1964; Stephens & Herberg 1975). Additionally, an anatomical mapping study conducted by Corbett and Wise (1980) found that EBS self-administration was best supported by placement of electrodes in parts of the VTA, a brainstem region containing dense populations of DA neurons. Collectively, these studies showed that DA neurotransmission was an important component of the brain circuitry that mediates the rewarding effects of EBS.

Concurrent with studies investigating EBS reward mechanisms, researchers began pursuing the idea that DA neurotransmission was also involved in mediating the rewarding effects of a variety of drug and natural rewards. The first indication that abused drugs tapped into the brain’s reward system came from the demonstration that amphetamine modulated responding for EBS (Stein 1964). Subsequently, it was shown that laboratory animals responded vigorously in an instrumental self-administration paradigm to receive injections of psychostimulant drugs (Pickens & Harris 1968). The possibility that direct activation of DA neurotransmission mediated the rewarding effects of psychostimulant drugs came from three separate lines of evidence. First, the DA receptor agonists apomorphine and piribedil sustained self-administration (Baxter et al 1974; Davis & Smith 1977; Wise et al 1976; Yokel & Wise 1978). Second, lesions to the ascending fibers of the DA pathway effectively eliminated the ability of psychostimulant drugs to sustain self-administration (Lyness et al 1979; Roberts et al 1977; Roberts et al 1980). Third and perhaps most striking was the ability of DA receptor antagonists to severely disrupt the prototypical high rates of instrumental responding for psychostimulant drugs and DA receptor agonists in the self-administration paradigm (Baxter et al 1974; Davis & Smith 1977; de Wit & Wise 1977; Risner & Jones 1976; Risner & Jones 1980; Wilson & Schuster 1972; Yokel & Wise 1975; Yokel & Wise 1976; Yokel & Wise 1978). For example, de Wit and Wise (1977) trained rats to lever press for cocaine and then tested these animals following pre-treatment with one of a wide range of doses of pimozide or saline. A very distinctive pattern of drug effects emerged in this study. Specifically, rats treated with the lowest dose of pimozide significantly increased their rate of responding compared to saline-treated rats, whereas rats treated with the high doses of pimozide dramatically increased their rate of responding at the outset of testing, but then eventually stopped responding altogether. The increased responding for cocaine observed in the rats treated with a low dose of pimozide suggested that the animals no longer found the previous dose of cocaine sufficiently rewarding since this behavioural pattern mirrored the commonly observed effect of lowering the dose of a psychostimulant drug. In this case, laboratory animals will increase their rate of responding in an effort to maintain a consistent blood level of the drug and to presumably optimize the drug’s rewarding effects. Additionally, the behavioural pattern of rats treated with high doses of pimozide, characterized by an initial robust increase in responding followed by a complete cessation of responding, resembled the extinction effect observed when animals previously trained to receive a reward are tested under conditions of non-reward. This pattern was also taken to suggest that the rewarding effects of cocaine were severely diminished by pre-treatment with a DA receptor antagonist. Combined with the growing evidence that neither lesions to the ascending fibers of the NE system (Roberts et al 1977) nor administration of NE antagonists (Davis & Smith 1975; Davis & Smith 1977; de Wit & Wise 1977; Risner & Jones 1976; Risner & Jones 1980; Yokel & Wise 1975; Yokel & Wise 1976; Yokel & Wise 1978) compromised self-administration of DA- augmenting drugs, it became clear that DA, but not NE, played an important role in mediating the rewarding effects of psychostimulant drugs. Following observations that DA receptor antagonists disrupted instrumental responding for natural rewards, such as food and water (Gerber et al 1981; Wise & Schwartz 1981; Wise et al 1978a; Wise et al 1978b), in much the same way that these drugs disrupted instrumental responding for artificial rewards, such as psychostimulant drugs and EBS, it appeared likely that DA neurotransmission was a common element in the brain circuitry that responded to nearly all rewards.

Wise (1982) integrated the findings from investigations into the effect of DA receptor antagonists on EBS, drug and natural reward and formulated the anhedonia hypothesis of DA’s involvement in reward. The main purpose of the anhedonia hypothesis was to explain the robust performance-lowering effect of DA receptor antagonists on instrumental responding for a variety of rewards. The major thrust of the hypothesis was that DA receptor antagonists profoundly altered an animal’s level of “motivational arousal” by disrupting the rewarding effects of unconditioned stimuli as well as conditioned stimuli associated with reward. By rewarding impact, Wise meant the ability of these stimuli to produce a hedonic reaction and to reinforce behaviours that led to the acquisition and consumption of the unconditioned stimulus. The hypothesis was developed on the basis of several major behavioural patterns that emerged from studies examining the effect of DA receptor antagonists on reward. First, the response pattern of animals following pre-treatment with DA receptor antagonists resembled that of animals tested under the condition of non-reward. Specifically, in extinction trials involving omission of a previously reinforced reward, normal drug-free animals will initially respond at a high rate, but after failing to receive the reward, these animals gradually cease to respond. The same response pattern was observed following pre-treatment with DA receptor antagonists despite the fact that the reward was still available. Wise argued that this similarity in response patterns, termed “extinction mimicry,” occurred because animals treated with DA receptor antagonists came to experience the reward the same way as a normal drug-free animal came to experience non-reward. In other words, it appeared that the reward had lost its hedonic value following treatment with DA receptor antagonists.

Results from studies involving psychostimulant drugs were particularly striking since consistently elevated rates of responding were observed in animals pretreated with low doses of DA receptor antagonists, while an initial large burst of responding followed by a complete cessation of responding was seen in animals pre-treated with high doses of DA receptor antagonists. This was taken to suggest that DA receptor antagonism reduced the rewarding effects of these drugs and, consequently, animals increased responding in order to acquire a higher dose of the drug and presumably achieve the same magnitude of rewarding effect that previously occurred at the lower drug dose. The effects of DA receptor antagonism on instrumental responding for reward also resembled two other phenomena observed following non-reward in normal, drug-free animals: spontaneous recovery and decreased resistance to extinction. The former refers to a renewal of high rates of responding at the beginning of a new test session following an extinction trial, while the latter refers to a cumulative reduction in responding over successive extinction trials. Again, the similar behavioural patterns were taken to support the proposition that animals treated with DA receptor antagonists essentially valued the reward as much as a normal drug-free animal valued non-reward. These features were also important because they helped to rule out the alternative hypothesis that DA receptor antagonists affected instrumental responding by impairing motor activity rather than altering reward function. Second, at least with natural rewards, animals required multiple exposures to reward while under the influence of a DA receptor antagonist before a performance decrement was observed (Mason et al 1980; Wise et al 1978a). Additionally, normal levels of instrumental responding could be reinstated in these same animals if they were tested in a drug-free condition that occurred between test sessions involving pre-treatment with a DA receptor antagonist (Mason et al 1980). Taken together, these results demonstrated that animals needed to experience the reward while under the influence of a DA receptor antagonist before the drug would impact instrumental responding for that reward. It appeared that animals decreased instrumental responding in this situation because the hedonic value of the reward was lower following DA blockade in comparison to a drug-free state. Third, decreased instrumental responding could be observed in the same animal following a transfer from several days of experience in a non-reward condition to a test session where the animal was pretreated with a DA receptor antagonist (Gerber et al 1981; Wise et al 1978a). This transfer effect was strongly suggestive of the existence of a shared property between the experience of non-reward and the experience of reward following pre-treatment with a DA receptor antagonist. Fourth, DA receptor antagonists also progressively diminish the ability of conditioned stimuli to elicit instrumental responding for reward (Gray & Wise 1980).

A major argument against the anhedonia hypothesis was that DA receptor antagonists disrupted instrumental responding for reward not through an effect on reward per se, but rather by compromising motor function (Fibiger et al 1976). However, this was essentially ruled out by the fact that high instrumental response rates were initially observed following pre-treatment with DA receptor antagonists and again during tests of spontaneous recovery. Moreover, in experiments specifically designed to separate motor and reward functions, motor activity only decreased in animals pre-treated with DA receptor antagonists following several trials of normal responding and, most importantly, experience with the reward (Fouriezos et al 1978; Wise et al 1978a).

Although the main intent of the anhedonia hypothesis was to account for DA’s role in reward as objectively measured by operant conditioning paradigms in laboratory animals, Wise and colleagues also openly speculated about a potential role of DA as a mediator of the subjective state of pleasure (Wise 1980; Wise 1982; Wise et al 1978b). This seemed to be a logical extension of the framework they presented to explain the modulatory effect of DA receptor antagonists on instrumental responding for reward, since hedonic reactions, including pleasure, presumably occur following interaction with rewards. This proposition also found some support from contemporary studies in humans, specifically the observations that DA receptor antagonists diminished amphetamine-induced euphoria in drug users (Gunne et al 1972; Jonsson 1972; Jonsson et al 1971) and induced dysphoria in some patients with schizophrenia (Singh 1976). Moreover, humans reported feeling pleasure-like effects following EBS of brain regions innervated by DA neurons (Heath 1972). Thus, by the beginning of the 1980s, several distinct lines of evidence were suggestive of a role of DA neurotransmission in mediating positive mood states, such as pleasure.

3.0  Dopamine and positive mood states

3.1  Pre-clinical evidence against the anhedonia hypothesis

With respect to DA’s involvement in pleasure, the anhedonia hypothesis was considered speculative. To the extent that it is possible to model and measure such subjective experiences in laboratory animals, none of the original experiments whose results form the basis of the anhedonia hypothesis actually did so. The proposition that DA mediated the pleasure associated with rewards mainly rested on the assumptions that pleasure always follows reward consumption and animals experience pleasure in the same way that humans do. Wise (1985) himself admitted this in a reformulation of the anhedonia hypothesis: «the assumption that pleasure is attenuated by neuroleptics is thus not a data-based assumption in the traditional sense. It is largely based on personal subjective experience; pleasure is a state which usually seems to accompany reward (Wise 1985, page 182).» Clearly, the question of what role, if any, DA plays in positive mood states needs to be answered with evidence from studies in humans. Nevertheless, recent pre-clinical research has helped address this question by striving to elucidate the exact nature of DA’s involvement in reward, motivation and hedonic processes.

Two lines of indirect evidence and one direct line of evidence have emerged from pre-clinical studies which cast doubt on the hypothesized role of DA as a mediator of positive mood states, including pleasure. First, the timing of DA neuron firing and DA release do not coincide with reward consumption. If DA mediated pleasure, DA neuron firing should occur just prior to, and DA release during, interaction with a reward that is currently being consumed since that is the time when pleasure would be expected to be maximal. Experimental findings, though, do not support this prediction. For example, DA release in the nucleus accumbens (NAcc), a region of the VS that is densely innervated by VTA DA neurons, typically increases and then peaks prior to consumption of food or drug reward (Gratton & Wise 1994; Kiyatkin & Gratton 1994; Kiyatkin & Stein 1996; Kiyatkin et al 1993; Phillips et al 1993; Richardson & Gratton 1996). Moreover, following multiple exposures, DA release begins to increase and then peak after presentation of visual or auditory cues that have been repeatedly paired with food or drug reward (Gratton & Wise 1994; Phillips et al 1993; Richardson & Gratton 1996). Similarly, electrophysiological studies have found that the firing rate of midbrain DA neurons does not increase following reward consumption, except when the reward is presented unexpectedly or during the initial stages of learning a task that involves reward (Ljungberg et al 1991; Ljungberg et al 1992; Mirenowicz & Schultz 1994; Schultz et al 1993; Schultz & Romo 1990). After extensive learning, midbrain DA neurons fire robustly and consistently to the presentation of cues associated with reward, but no increases in the firing rate are observed in response to the reward itself (Ljungberg et al 1991; Ljungberg et al 1992; Mirenowicz & Schultz 1994; Schultz et al 1993; Schultz & Romo 1990). Second, a growing body of evidence implicates DA in aversive motivation (Ikemoto & Panksepp 1999; Salamone 1994a). Briefly, DA is released in the NAcc in response to a variety of aversive stimuli or stressful conditions, including foot or tail shock, tail pinch, restraint, forced exercise and anxiogenic drugs (Abercrombie et al 1989; Bertolucci-D’Angio et al 1990; D’Angio et al 1987; Imperato et al 1992; Imperato et al 1991; Kalivas & Duffy 1995; McCullough & Salamone 1992; Scatton et al 1988; Sorg & Kalivas 1991; Young et al 1993). Similar to reward-predicting conditioned stimuli, cues that are repeatedly presented in association with aversive stimuli also come to elicit DA release in the NAcc (Young et al 1993). Moreover, DA receptor antagonists impair avoidance responding (Ader & Clink 1957; Beninger et al 1980; Cook & Weidley 1957;

Davidson & Weidley 1976; White et al 1992). Taken together, these findings demonstrate that DA neurotransmission is not uniquely involved in reward processing or appetitive motivation.

The biggest pre-clinical challenge to the proposition that DA is a neurochemical mediator of pleasure has come from a series of studies using the taste reactivity test, which assesses the affective responses of animals after ingestion of sweet and bitter solutions. Briefly, the pattern of orofacial responses typically observed after an animal ingests a sweet solution are thought to reflect a positive evaluation akin to «liking» (hedonic reactions) whereas orofacial responses observed after an animal ingests a bitter solution are thought to reflect a negative evaluation akin to «disliking» (aversive reactions; Berridge & Robinson 1998). Similar orofacial responses are observed across species, including humans (Berridge & Robinson 1998). Though it allows for a more direct assessment of how neurotransmitters, such as DA, affect hedonic processes in animal models, it is important to note that the taste reactivity test is not an index of subjective pleasure. In humans, orofacial responses to taste stimuli are highly correlated with subjective ratings of «liking» and «disliking,» but they also occur normally in anencephalic infants (Berridge 1996; Steiner 1973). These and other findings suggest that the neural mechanisms underpinning orofacial responses to taste stimuli might be independent from those that mediate subjective hedonic experiences. Thus, while the taste reactivity test is a useful tool to investigate the neurobiology of basic hedonic processes, it can only provide limited insight into the role of DA in positive mood states, which are inherently subjective experiences.

With this caveat aside, several studies have examined the influence of experimentally-altered DA neurotransmission on positive and negative affect as measured by the taste reactivity test. According to the anhedonia hypothesis, methods that augment DA neurotransmission should increase hedonic reactions to sweet tastes, whereas methods that attenuate DA neurotransmission should do the opposite. The pattern of results, however, contravenes these predictions. DA augmenting drugs, such as amphetamine and apomorphine, do not increase the number of hedonic reactions (Tindell et al 2005; Treit & Berridge 1990; Wyvell & Berridge 2000), nor does a robust elevation of DA levels with a hyperdopaminergic DAT knockout mouse (Pecina et al 2003). DA receptor antagonists, such as pimozide and haloperidol, fail to decrease the number of hedonic reactions (Pecina et al 1997; Treit & Berridge 1990) as do neurochemical-induced lesions of DA projections that substantially deplete DA levels (Berridge & Robinson 1998; Berridge et al 1989). Collectively, these findings suggest that DA neurotransmission is not involved in the neural mechanisms that underpin basic hedonic processes.

3.2  Neuropsychiatric disorders and mood

Three neuropsychiatric disorders in which DA dysfunction is thought to be a component of the disease pathophysiology provide some insight into the potential role of DA neurotransmission in mood. First, altered DA neurotransmission has been implicated in the pathophysiology of depression and bipolar disorder, though no simple association between low DA levels and depressive symptoms has been demonstrated (Dunlop & Nemeroff 2007; Leyton 2009). Rather, there is some evidence to suggest that DA dysfunction is present in a sub-group of depressed patients who exhibit psychomotor retardation (Meyer et al 2001; Meyer et al 2006). Second, PD, which involves pronounced decreases in DA neurotransmission and profound motor deficits, is also associated with mood and motivational disturbances (Aarsland et al 2005; Weintraub et al 2005). These latter symptoms likely emerge secondary to motor problems and are typically ameliorated with DA replacement therapy. Intriguingly, a small percentage of medicated PD patients develop a hypomanic-like syndrome, commonly called «DA dysregulation syndrome» (DDS), which is characterized by mood elevation, compulsive drug-taking and dramatic increases in goal-directed behaviours (Giovannoni et al 2000). As with bipolar mania, the precise contribution of increased DA neurotransmission to positive mood is not entirely clear. However, one recent study with PD patients found an association between the magnitude of L-DOPA-induced DA release in the VS and subjective ratings of «drug wanting,» but not «drug liking,» suggesting that augmented DA neurotransmission does not contribute directly to the increased positive mood observed in PD patients with DDS (Evans et al 2006). Third, patients with schizophrenia, a psychiatric disorder thought to involve abnormally elevated striatal DA neurotransmission, do not experience euphoria as the anhedonia hypothesis would predict. However, these patients often complain of lowered mood and motivation following treatment with antipsychotic drugs, an effect sometimes referred to as «neuroleptic-induced dysphoria» (Lewander 1994; Singh 1976; Singh & Smith 1973) and these symptoms correlate with the degree of medication-induced DA D2 receptor blockade (Bressan et al 2002; de Haan et al 2000; Mizrahi et al 2007). Collectively, these lines of clinical evidence provide only weak support for the proposition that DA neurotransmission is involved in mood regulation.

3.3  Dopaminergic agents: selectivity and mechanisms of action

DA neurotransmission can be experimentally increased in humans through the administration of a variety of drugs. For the purpose of this review, these drugs will be divided into three main classes: specific DA augmenters, nonspecific DA augmenters and DA receptor agonists. In comparison to the nonspecific DA augmenters, drugs such as L-DOPA and tolcapone are relatively devoid of effects on neurotransmitters other than DA. L-DOPA, the gold standard in the treatment of PD, is the immediate metabolic precursor to DA. L-DOPA administration increases DA synthesis in the brain, though the magnitude of this effect is more pronounced in animal models of PD compared to healthy intact animals (Rodriguez et al 2007). Surprisingly, L-DOPA administration does not appear to have a significant effect on NE synthesis in vivo in laboratory animals (Bartholini et al 1969; Butcher & Engel 1969; Doshi & Edwards 1981; Goshima et al 1991; Schoenfeld & Uretsky 1973). Tolcapone elevates synaptic levels of DA through its inhibition of COMT, an enzyme that degrades catecholamines

[1] History of Medicine, Hebrew University Medical Faculty, P.O. Box 12272, Jerusalem 91120, Israel;

I     wish to heartily thank Timothy J. Crow, Jaak Panksepp, Larry Stein, and Roy Wise for numerous conversations and e-mail exchanges regarding their scientific research and contributions during and following the period under study in this essay. I am also very grateful for the comments and suggestions of my fellow coeditors, the anonymous reviewers, and the editor of Osiris.

1      “Analysis of NIH Program Activities: Project Description Sheet,” p. 1. Principal Investigator: John C. Lilly, December 1955, folder 18, box 29, John C. Lilly Papers, Record ID M0786. Courtesy of Department of Special Collections and University Archives, Stanford University Libraries (hereafter JCL).

2 Isaac Asimov, The Human Brain: Its Capacities and Functions (1963; repr., New York, 1965), 188.

[2]      For an explanation of the “arrangement” that Magoun was referring to, see below. H. W. Magoun, “The Law of Effect: From Thorndike, to Skinner, to Olds” (1981), p. 10, folder 19, box 30, Magoun, Horace Winchell Papers, Manuscript Collection no. 140, Neuroscience History Archives, History and Special Collections for the Sciences, University of California, Los Angeles, Library Special Collections (hereafter HWM).

[3]      Unlike “emotions,” which were often studied in animals, the study of “pleasure” since the nineteenth century was confined almost exclusively to human subjects.

[4]      On Kantian, Burkian, and Humean aesthetics, see Laura Frost, The Problem with Pleasure: Modernism and Its Discontents (New York, 2013), Kindle edition; Catherine Cusset, No Tomorrow: The Ethics of Pleasure in the French Enlightenment (Charlottesville, Va., 1999); Regenia Gagnier, The Insatiability of Human Wants: Economics and Aesthetics in Market Society (Chicago, 2000). On Hobbes, Whytt, and the historical roots of modern hedonism, see Roy Porter, “Enlightenment and Pleasure,” in Pleasure in the Eighteenth Century, ed. Roy Porter and Marie Mulvey Roberts (London, 1996), 1-18; Ian Small, £gnditwn£jgrm£ritiei£m:AMhor;ity.£no№!£d££,.and.Lt£iayr&£L!t£ Nineteenth Century (Oxford, 1991). On the individualization of pleasure, see Colin Mercer, “A Poverty of Desire: Pleasure and Popular Politics,” in Formations of Pleasure, ed. Formations Collective (London, 1983), 84-100, on 91; emphasis in the original. See also Lynn Hunt and Margaret Jacob, “The Affective Revolution in 1790s Britain,” Eighteenth-£entm£ty&— 34 (2001): 491-521.

(Chicago, 2013). On the “pathologization of emotions,” see Frank Biess and Daniel Gross, eds., Sciencea»d£mo^3^s.Sft£L^945^A.Tra2SSt1a2iiC^£££2S£tiVelChi£^»2, 2014), 3. On Freudianism in the United States, see Alfred I. Tauber, “Freud’s Social Theory: Modernist and Postmodernist Revisions,” HieLMumSei— 25 (2012): 43-72; Dorothy Ross, “AHR Roundtable: American Modernities, Past and Present,” Amer.Hist.Rev. 116 (2011): 702-14. On Dichter, see Stefan Schwarzkopf and Rainer Grie, eds.,ErnestDiehterandMotivationResearch:^fewPerspeetiveson.the Maknge£Pest-War.C£nsumeL,Culture (Basingstoke, 2010). For the notion of the “long” 1960s, see John Carlevale, “The Dionysian Revival in American Fiction ofthe Sixties,” LJ£T 12 (2006): 364-91. Carlevale is following Arthur Marwick in adopting this periodization. On the contradictions and transformations ofthe 1960s, see Howard Brick, The Age of Contradiction: American Thought and Culture in the 1960s (Ithaca, N.Y., 1998), 1-22; Marianne DeKoven, Utopia Limited: The Sixties and the Emergence of the Postmodern (Durham, N.C., 2004).

[6]1 bracket the ethical critiques that emerged in retrospect in regard to some of the experiments that were carried out in the context of the study of pleasure. For this latter ethical critique, see Christina Kathryn Fradelos, “The Last Desperate Cure: Electrical Brain Stimulation and Its Controversial Beginnings” (PhD diss., Univ. of Chicago, 2008).

[7]      E. Boring to Stratton, 8 March 1926, nAs-NRC Archives Div A&P Rec Grp: DNRC: A&P: “Conf on Experimental study of Human Emotions: Second,” 1926 March, Washington, D.C.

[8]      Other historians have provided succinct summaries and reviews of some of the major scientific developments that led to the new discoveries. These included the research on deep brain stimulation by the Nobel laureate W. R. Hess, the anatomical and physiological contributions of S. W. Ranson, the discovery of the Reticular Activating System by W. H. Magoun and G. Moruzzi, and the elucidation of hypothalamic control of drives. For a well-informed history of reward, see Lawrence E. Marks, “A Brief History of Sensation and Reward,” in Neurobiology of Sensation and Reward, ed. J. A. Gottfried (Boca Raton, Fla., 2011), (accessed 13 December 2013). For the historical background, see Alan A. Baumeister, “Serendipity and the Cerebral Localization of Pleasure,” JHsLMeMesCi— 15 (2006): 92-8; Henry J. de Haan, “Origins and Import of Reinforcing Self-Stimulation ofthe Brain,” JHislLNeynSsei— 19 (2010): 24-32; John Gardner, “A History of Deep Brain Stimulation: Technological Innovation and the Role of Clinical Assessment Tools,” Soc. Stud. Sci. 43 (2012): 707-28.

[9]      However, I emphasize throughout my analysis that a history in terms of “reward” is essential for writing the complete history of “pleasure” (and reward). This essay is the first installment in a broader project on the scientific and cultural histories of postwar pleasure and reward in the sciences—The Sciences and Cultures of Pleasures and Rewards. The study ofpleasure and reward generated an enormous number of publications. In the footnotes that follow, I provide only a few exemplary references out of many.

[10]     Dr. M. E. Olds, e-mail message to Otniel E. Dror, 10 July 2014. I am grateful to Dr. M. E. Olds, James Olds’s spouse and part-time collaborator, for her personal reminiscence of the fateful day of discovery. Dr. Olds passed away several weeks after our e-mail exchange.

[11]     Originally published in 1949, Hebb’s The Organization of Behavior was a major contribution to the neurophysiology of behavior and to a more general attempt to neurophysiologize psychology. See D. O. Hebb’s The Organization of Behavior: A Neuropsychological Theory (1949; repr., New York, 1959).

[12]     This shift was emphasized by many investigators. See, e.g., Donald B. Lindsley, “Physiological Psychology,” AnauLRsvLPsyshsl— 7 (1956): 323-48; Eliot Stellar, “Physiological Psychology,” Annu. Rev. Psychol. 8 (1957): 415-36.

[13]     James Olds, “Physiological Mechanisms of Reward,” in Nebraska Symposium on Motivation, ed. Marshall R. Jones (Lincoln, Neb., 1955), 73-147, on 84.

[14]     Some suggested that the stimulus was turning brain activity off rather than on. Others suggested that the stimulus was activating the viscera, and feedback from the viscera was “pleasurable.” Still others proposed that the stimuli had an anesthetic effect and alleviated pain, rather than producing reward. Other investigators suggested that the stimulus induced a seizure in the brain, which in and of itself, irrespective of reward, increased the number of lever presses. For the citation, see Peter M. Milner, “The Discovery of Self-Stimulation and Other Stories,” Nguo£L.&B£b£ha!vLRv 13 (1989): 61-7, on 63.

[15] James Olds, “Pleasure Centers in the Brain,” Eng. & Sci. 33 (1970): 22-31, on 26. This was a criticism that had been suggested by Miller.

[16]     Some, like Miller, continued to suggest models that retained drive reduction, without rejecting Olds’s findings. See “Dr. Neal E. Miller, Comments on the Implications of the Olds Reward Effect for Theories of Reinforcement, 1956,” folder 62, box 8, HWM.

[17]     I emphasize here both the discovery of “pleasure” and its discovery in the brain.

[18] O. H. Mowrer, “Motivation,” Annu. Rev. Psychol. 3 (1952): 419-38, on 419.

[19]     Abraham Maslow, “Deficiency Motivation and Growth Motivation,” in Jones, Nebraska Symposium (cit. n. 14), 1-30, on 10-3.

[20]     On the history of pleasure, and for “negation of a negation,” see Frost, The Problem with Pleasure, 8. See also Cusset, No Tomorrow (both cit. n. 5).

[21]     For the shift from “pathway” to “circuit,” see Anthony G. Phillips and Gordon J. Mogenson, “Brain-Stimulation Reward: Current Issues and Future Prospects,” CaLJPychQL— 32 (1978): 124-8, on 125. These shifts in the geometry of pleasure, from brain“center(s)” to “circuit(s),” were highly significant.

[22]     The remaining 60 percent was neutral. For these estimates, see James Olds, “Differentiation of Reward Systems in the Brain by Self-Stimulation Technics,” in Electrical Studies on the Unanesthetized Brain, ed. Estelle R. Ramey and Desmond S. O’Doherty (New York, 1960), 17-51, on 18.

[23]     On Deleuze, see Frost, The Problem with Pleasure, 11. See also Cusset, No Tomorrow (both cit. n. 5).

[24]     Skinner took the term “reinforcement” from Pavlov. See B. F. Skinner to Roy A. Wise, 2 December 1986. I thank Roy Wise for sharing this letter with me.

[25]     Within the “reward” camp, there were also disagreements. Some investigators, e.g., argued that “reward” and “punishment” were already too value laden. See Howard S. Liddell, James Olds, and Roger W. Sperry, “Post-Pavlovian Development in Conditional Reflexes,” in The Central Nervous System and Behavior, ed. M. A. B. Brazier (New York, 1959), 211-31.

[26]      “Analysis of NIH Program Activities” (cit. n. 1).

[27] For “pleasure” in Olds’s publications, see, e.g., Olds, “Physiological Mechanisms” (cit. n. 14); Olds, “Pleasure Centers in the Brain,” ScLAmeL 195 (1956): 105-16; Olds, “Self-Stimulation of the Brain,” Science 127 (1958): 315-24; Olds, “Pleasure Centers,” 1970 (cit. n. 16).

[28]     “Neurones, synapses, or any other aspect of the internal economy of the organism … lie outside the field of behavior as here defined.” See B. F. Skinner, The Behavior of the Organisms: An Experimental Analysis (New York, 1938), 418.

[29]     See, e.g., D. B. Macfarlane, “McGill Opens Vast New Research Field with Brain ‘Pleasure Area’ Discovery,” Montreal Star, 12 March 1954, 1-2; Robert Coughlan, “Part I: Behavior by Electronics,” Life 64 (8 March 1963): 90-106; Olds, “Pleasure Centers,” 1956 (cit. n. 28); Asimov, The Human Brain (cit. n. 2); J. Anthony Deutsch, “Brain Reward: ESB and Ecstasy,” Psychology Today 6 (1972): 45-9.

[30]     James Olds, “Commentary,” in Brain Stimulation and Motivation: Research and Commentary, ed. Elliot S. Valenstein (Glenview, Ill., 1973), 81-99, on 85.

[31]     This authentication already appeared in the first ever publication to demonstrate that direct stimulation of the brain produced an authentic “aversive” reaction, rather than mere motor-reflex movements. This first study, by Delgado, Miller, and Roberts of Yale University, set the stage for Olds’s discovery of authentic brain-induced pleasure-reward. This first study was also significant since it challenged Karl Lashley’s and Jules Masserman’s determination that brain-induced aversive reactions and emotions were mere reflex motor movements, since, as they argued, they could not be conditioned and could not be used to motivate learning. Delgado, Roberts, and Miller demonstrated that direct stimulation of the brain could produce emotional conditioning and motivate learning of instrumental responses. See Jose M. R. Delgado, Warren W. Roberts, and Neal E. Miller, “Learning Motivated by Electrical Stimulation of the Brain,” Amer. J. Physiol. 179 (1954): 587-93.

[32]     The pleasure of laboratory rats immediately preceded the imminent emergence of an ethics of pain and pleasure in animal ethics during the late 1960s and early 1970s. The new animal ethics was distinguished from previous animal ethics in emphasizing and valuing the pleasure/well-being of animals, beyond the elimination/reduction of animal pain and suffering, which had dominated previous approaches to nonhuman animals. See Peter Singer’s Animal Liberation (New York, 1975) as the most obvious example. See also the important publications on pleasure in animals by both Michel Cabanac and Jaak Panksepp.

[33]     The all-or-none principle of nerve action undergirded the interpretation of electrical brain stimulation particularly and crucially during the early cartographic-mapping phase of pleasure in the brain. The study and identification of different neurotransmitters would be crucial from the 1960s onward. The firing rates of neurons would be important for pinpointing the neurons that were significant for pleasure/reward and excluding others.

[34]     For “purely rewarding,” see, e.g., John C. Lilly, “The Psychophysiological Basis for Two Kinds ofInstincts: Implications for Psychoanalytic theory,” JAmeiLPsychOOnalyLAsSOC— 8 (1960): 659-70, on 667.

[35] For “supramaximal,” see John C. Lilly, “LSD: Reward and Punishment,” undated, folder 3, box 28, JCL. For “super-pleasure,” see William H. Davis, “The Pleasure Helmet and the Super Pleasure Helmet,” J- Thought 10 (1975): 290-3; Sandor Rado, “Fighting Narcotic Bondage and Other Forms of Narcotic Disorder,” Compshen£^££chiat— 4 (1963): 160-7.

[36]     On this problem, see, e.g., Elliot S. Valenstein, “Problems of Measurement and Interpretation with Reinforcing Brain Stimulation,” PsychoLRev. 71 (1964): 415-437.

[37]     For “pleasure centers,” see Olds, “Pleasure Centers,” 1956 (cit. n. 28); Olds, “Pleasure Centers,” 1970 (cit. n. 16).

[38]      Lilly, “LSD” (cit. n. 36), 2.

[39]     John C. Lilly, “Some Considerations Regarding Basic Mechanisms of Positive and Negative Types of Motivations,” AmerJPsychiat. 115 (1958): 498-504, on 501. As Lilly explained, dolphins are a species that must remain conscious in order to continue breathing. For extensive background on Lilly and his research on dolphins, see D. Graham Burnett, The Sounding of the Whale: Science and Cetaceans in the Twentieth Century (Chicago, 2012).

[40]     James Olds, “Pleasure and Value,” XVth International Congress of Psychology, Acta Psychol. 15 (1959): 76-7, on 76. This discovery, Olds noted, would also establish “an experimental psychology of positive motivation” (77).

[41]     Olds, “Pleasure Centers,” 1956 (cit. n. 28), 110.

[42]     Milner, “The Discovery” (cit. n. 15), 64.

[43]     Elliot S. Valenstein, Brain Control: A Critical Examination of Brain Stimulation and Psychosurgery (New York, 1973), 67-8.

[44]     For a different example of how “failure” can contribute to the evolving understanding of affect, see Eric J. Engstrom, “Tempering Madness: Emil Kraepelin’s Research on Affective Disorders,” in this volume.

[45]     Roderic Gorney, “The New Biology and the Future of Man,” UCLA Law Rev. 15 (1967-8): 273356, on 338. There is no explanation for why the dolphin died.

[46] Larry Niven, “Death by Ecstasy,” Galaxy Magazine 27 (1969), /Death%20by%20Ecstasy%20-%20Larry%20Niven.txt (accessed 1 June 2016).

[47] J. Olds, R. P. Travis, and R. C. Schwing, “Topographic Organization of Hypothalamic SelfStimulation Functions,”   53 (1960): 23-32, on 27.

[48]     PHS-NIH, Individual Project Report, “Mapping the Behavior Elicitable by Electrical Stimulation of the Brain,” 1957, folder 18, box 29, JCL.

[49]      Roy Wise, e-mail message to Otniel E. Dror, 19 September 2014.

[50]     “Discussion between Dr. Sidney Cohen and Dr. Lilly,” p. 2, 10 February 1967, folder 6, box 44, JCL.

[51]     See, e.g., Valenstein, Brain Control (cit. n. 44); Coughlan, “Behavior by Electronics” (cit. n. 30). Some, but not all, of these reports should be read in the context of attempts to assuage public fears— by showing that humans, e.g., can resist this type of control.

[52]     For a direct critique of Ryle’s argument, which drew directly on Olds’s experiments, in arguing against Ryle’s assertion that “pleasure is not a sensation because, inter alia, it is not separable from its source, a cause or effect, clockable or locatable or describable the way pains are,” see, e.g., Roland Puccetti, “The Sensation of Pleasure,” BriLJ.PhiL.Sci— 20 (1969): 239-45, on 239.

[53]     Paul E. Meehl, “Psychology and the Criminal Law,” Univ. Richmond Law Rev. 5 (1970): 1-30, on 13.

[54]     This quotation from Carol Tavris appeared in Deutsch, “Brain Reward” (cit. n. 30), 45. Deutsch was one of the leading investigators of EBS and reward.

[55]     The quotations are, respectively, from Albertus Haller, First Lines of Physiology, ed. Lester S. King (1786; repr., New York, 1966), 80; Charles S. Sherrington, The Integrative Action of the Nervous System (New Haven, Conn., 1906), 333.

[56]     For the (hypo)thalamus as the locus of the “id,” see Walter B. Cannon to Carl A. L. Binger, 24 October 1934, folder 1529, box 110, Walter Bradford Cannon Papers (H MS c40), Harvard Medical Library in the Francis A. Countway Library of Medicine, Boston, Mass.

[57]     “Temperature regulation” is not italicized in the text. I emphasize it here in order to stress Maslow’s perceptive nondistinction between the super-pleasure of copulating, eating, and temperature regulation. I will return to this below in discussing “missed” polymorphous pleasures. For the citation, see Olds, “Physiological Mechanisms” (cit. n. 14), 145-6.

[58] Davis, “The Pleasure Helmet” (cit. n. 36). I note that Robert Nozick’s contemporaneous and renowned “Experience Machine” did not allude to Olds’s rats. See Nozick, “The Experience Machine,” in Anarchy, State, and Utopia (1974; repr., Oxford, 1999), 42-5.

[59]     Kant distinguished between high and low pleasures, high and low aesthetics, and the sensual vs. the reflective. For these distinctions, see Noel B. Jackson, “Rethinking the Cultural Divide: Walter Pater, Wilkie Collins, and the Legacies of Wordsworthian Aesthetics,” Mod^hilgl. 102 (2004): 207-34; for the citation, see Frost, The Problem with Pleasure (cit. n. 5), 9.

[60]     For a concerted attempt to come to terms with the neurophysiological discovery/argument that all pleasures are “low,” see H. J. Campbell, The Pleasure Areas (London, 1973).

[61]     On the emergence, contexts, and history of “brainwashing,” see David Seed, Brainwashing: The Fictions and Mind Control: A Study of Novels and Films (Kent, Ohio, 2004). “Brainwashing” was coined by Edward Hunter in 1950. Huxley’s Brave New World (Revisited) figured prominently in the Cold War literature on brainwashing. See Vance Packard, The Hidden Persuaders (New York, 1977).

[62]     Jose M. R. Delgado, Physical Control of the Mind: Toward a Psychocivilized Society (Evanston, Ill., 1969).

[63]      Lilly, “LSD” (cit. n. 36), 7; emphasis in the original.

[64]     Quality of Health Care—Human Experimentation, 1973 Hearings before the Subcommittee on Health of the Committee on Labor and Public Welfare, United States Senate, Ninety-Third Congress, First Session, 370.

[65]      Niven, “Death by Ecstasy” (cit. n. 47).

[66]     On plaisir and jouissance and their respective conformity with and disruption of the dominant ideology, see, in particular, Brian L. Ott, “(Re)Locating Pleasure in Media Studies: Toward an Erotics of Reading,” Comm. Crit. Cult. Stud. 1 (2004): 194-212.

[67]     This subtitle invokes Herbert Marcuse’s contemporaneous “polymorphous perversity” or “polymorphous sexuality” in Eros and Civilization. The term originated in Freud’s studies of infantile sexuality. See Marcuse, Eros and Civilization: A Philosophical Inquiry into Freud (1955; repr., Boston, 1966).

[68]     Cora Kaplan, “Pleasure/Sexuality/Feminism,” in Formations Collective, Formations of Pleasure (cit. n. 5), 15-35, on 15.

[69]     This was in stark contrast to the Freudian-inspired motivation research of Ernest Dichter.

[70]     This nondistinction is obvious in numerous publications from this earlier period. Larry Stein, one of the leading investigators during this early period, affirms that in numerous experiments the investigators were indifferent to the drive specificity of the “reward.” Stein, telephone conversation with Otniel E. Dror, 10 October 2014.

[71]     For the community of experimenters, the more significant direct links with drugs would be forged during the 1970s.

[72]      See the references in n. 30.

[73]     Judith Hooper, “John Lilly: Altered States,” Omni Magazine (January 1973), https://www (accessed 5 July 2014).

[74] Maslow continued: “I suppose Olds and Hebb will be horrified by this kind of speculation.” See Olds, “Physiological Mechanisms” (cit. n. 14), 147.

[75]     For a fuller discussion, see Otniel E. Dror, The Sciences and Cultures of Pleasures and Rewards (manuscript, History of Medicine, Hebrew University).

[76]     EBS reward had an extremely fast extinction rate, it often required “priming” the animal, it was debatable whether it could be used for secondary conditioning, and more.

[77]      Miller, “Comments” (cit. n. 17).

[78]      Olds, “Pleasure Centers,” 1970 (cit. n. 16), 30.

[79]      Ibid.

[80]      For the various citations, see ibid., 22, 31.

[81]    This postwar shift to abundance-affluence was highly differentiated and discriminatory in postWorld War II United States society. There is an abundant literature on the shift from scarcity to abundance and its implications for numerous post-World War II developments. See, e.g., Brick, The Age of Contradiction (cit. n. 6).

[82]1 am drawing here on Raymond Williams’s pointed analysis of the historical conjunction between “revolution” in terms of revolving in space and “revolution” in terms of a political rebellion. See Williams, Keywords: A Vocabulary of Culture and Society (1976; repr., New York, 1983), 270 -4.

[83]      Roy Wise, telephone conversation with Otniel E. Dror, 5 September 2014.

[84]     For an analysis that also emphasizes practices in consolidating a new affective ontology, see Felicity Callard, “The Intimate Geographies of Panic Disorder: Parsing Anxiety through Psychopharmacological Dissection,” in this volume.

[85]     For the citation, see Jessica Lynn Grogan, “A Cultural History of the Humanistic Psychology Movement in America” (PhD diss., Univ. of Texas at Austin, 2008), 105-6.

[86]     Pleasure, however, was never really pure. Even at its source, it was corrupted and contaminated, since it was always embodied in distinct drives that diminished its true virtuous purity. The perpetuum itself could often be manipulated at its source through these specific drives— e.g., by changing levels of androgen (sex-reward perpetuum) or levels of satiety (feeding-reward perpetuum).

[87]1 note that in transposing this design to humans in terms of, e.g., “pleasure helmet” or otherwise, the workaholic rat was replaced by an automated super-pleasure generator that automatically stimulated the human brain and provided for “easy” passive pleasures.

[88]     For G. Stanley Hall and “laboratory hermits,” see Laurence R. Veysey, The Emergence of the American University (Chicago, 1965), 151.

[89]     For further elaborations, see Otniel E. Dror, Repetitions: For Science and for Pleasure (manuscript, History of Medicine, Hebrew University).

[90]     During its formative years, this was a science of inserting electrodes into brains and then stimulating and recording behaviors. This partly explains the relatively frequent reports of serendipity: one was never absolutely sure what the behavior of the animal would be during stimulation and where the electrode ended up in the brain until the post hoc dissection of the brain. This empiricism was accentuated by the fact that in the rat’s small brain, major distinct function centers were located in very close proximity to one another.