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Psychol Well Being. 2011 October 24; 1(1): 1–3. doi:10.1186/2211-1522-1-3.
Building a neuroscience of pleasure and well-being

Kent C Berridge1,* and Morten L Kringelbach2,3,*
1Department of Psychology, University of Michigan, Ann Arbor, USA
2Department of Psychiatry, Warneford Hospital, University of Oxford, Oxford, UK

3Centre for Functionally Integrative Neuroscience (CFIN), University of Aarhus, Aarhus, Denmark
Abstract
Background—How is happiness generated via brain function in lucky individuals who have the
good fortune to be happy? Conceptually, well-being or happiness has long been viewed as
requiring at least two crucial ingredients: positive affect or pleasure (hedonia) and a sense of
meaningfulness or engagement in life (eudaimonia). Science has recently made progress in
relating hedonic pleasure to brain function, and so here we survey new insights into how brains
generate the hedonic ingredient of sustained or frequent pleasure. We also briefly discuss how
brains might connect hedonia states of pleasure to eudaimonia assessments of meaningfulness, and
so create balanced states of positive well-being.
Results—Notable progress has been made in understanding brain bases of hedonic processing,
producing insights into that brain systems that cause and/or code sensory pleasures. Progress has
been facilitated by the recognition that hedonic brain mechanisms are largely shared between
humans and other mammals, allowing application of conclusions from animal studies to a better
understanding of human pleasures. In the past few years, evidence has also grown to indicate that
for humans, brain mechanisms of higher abstract pleasures strongly overlap with more basic
sensory pleasures. This overlap may provide a window into underlying brain circuitry that
generates all pleasures, including even the hedonic quality of pervasive well-being that detaches
from any particular sensation to apply to daily life in a more sustained or frequent fashion.
Conclusions—Hedonic insights are applied to understanding human well-being here. Our
strategy combines new findings on brain mediators that generate the pleasure of sensations with
evidence that human brains use many of the same hedonic circuits from sensory pleasures to
create the higher pleasures. This in turn may be linked to how hedonic systems interact with other
brain systems relevant to self-understanding and the meaning components of eudaimonic

happiness. Finally, we speculate a bit about how brains that generate hedonia states might link to
eudaimonia assessments to create properly balanced states of positive well-being that approach
true happiness.
Background
From Aristotle to contemporary positive psychology, well-being or happiness has been
usefully proposed to consist of at least two ingredients: hedonia and eudaimonia (Aristotle
© 2011 Berridge and Kringelbach; licensee Springer.

*
Correspondence: [email protected]; Morten. [email protected].
Authors’ contributions The authors contributed equally to this work
Competing interests The authors declare that they have no competing interests.
Publisher's Disclaimer: This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided
the original work is properly cited.
Berridge and Kringelbach Page 2
2009; Seligman et al. 2005). While definitions of these by philosophers and psychologists
have varied, most generally agree that hedonia at least corresponds psychologically to a state
of pleasure. Thus a particularly important topic for hedonic psychology and affective
neuroscience is to understand how pleasure is generated by brain mechanisms so as to

contribute to well-being. Fortunately, deciphering hedonia in the brain is a task in which
considerable progress has already been made. Eudaimonia by comparison may be more
difficult to define philosophically or approach scientifically, but most agree it corresponds to
some cognitive and/or moral aspect of a life lived well and not to any mere emotional
feeling. We view eudaimonia to mean essentially a life experienced as valuably meaningful
and as engaging. Thus, for psychological neuroscience of the future another major goal will
be to uncover how such experiences are reflected in patterns of brain activity (Urry et al.
2004).
Conceptually, hedonic processing and eudaimonic meaningfulness are very different from
each other. Yet, empirically, in real people well-being has been found to involve both
together. High questionnaire scores for hedonia and eudaimonia typically converge in the
same happy individual (Diener et al. 2008; Kuppens et al. 2008). That is, if a person self-
reports to be hedonically happy, then that same person is also likely to report a high sense of
positive meaningfulness in life. For example, in happiness surveys, over 80 percent of
people rate their overall eudaimonic life satisfaction as “pretty to very happy”. Comparably,
80 percent also rate their current hedonic mood as positive (for example, positive 6-7 on a
10 point valence scale, where 5 is hedonically neutral (Diener et al. 2008; Kuppens et al.
2008). A lucky few may even live consistently around a hedonic point of 8. Beyond that,
however, there may be such a thing as being too happy. Excessively higher hedonic scores
above 8 may actually impede eudaimonic attainment of life success, however, as measured
by wealth, education, or political participation (Oishi et al. 2007).
The tendency of pleasure and meaningfulness ratings to cohere together opens a potential
window of opportunity to the neuroscientific study of both aspects of well-being
(Kringelbach and Berridge 2009; Urry et al. 2004). If both hedonia and eudaimonia co-occur
in the same happy people, then identifying neural markers of one may give a toehold into
identifying the other. Still, most would probably agree that eudaimonic happiness poses
harder challenges to psychology and neuroscience. It is difficult even to define life
meaningfulness in a way as to avoid dispute, let alone to tie a happy sense of
meaningfulness to any specific brain patterns of activation. The difficulties of approaching
eudaimonic meaning are not insurmountable in principle, but for the foreseeable short term
seem likely to remain obstacles to affective neuroscience.
Therefore here we will focus mostly upon the hedonia or pleasure aspect of well-being. The
pleasure aspect is most tractable, and can be inspected against a growing background of
understanding of the neural foundations for specific pleasures. Supporting a hedonic
approach to happiness, happy people typically feel more pleasure in life. Indeed it has been
suggested that the best and simplest measure of well-being may be to merely ask people how
they hedonically feel right now–again and again–so as to track their hedonic accumulation
across daily life (Kahneman 1999). Such repeated self-reports of hedonic states could also
be used to identify more stable neurobiological hedonic brain traits that dispose particular
individuals toward happiness. Conversely, it will probably not be much disputed that the
capacity for pleasure is essential to normal well-being. Pathological loss of pleasure can be
devastating, and precludes well-being. Our aim is to use findings from recent research on
brain mechanisms of pleasure to ask how to higher states of hedonia might be generated to
produce well-being, and conversely what might go wrong in affective disorders (Berridge
and Kringelbach 2008; Kringelbach and Berridge 2010; Leknes and Tracey 2010; Smith et
al. 2010).

We note in passing that our focus on the hedonia component of happiness should not be
confused with hedonism, which is the pursuit of pleasure for pleasure’s own sake, and more
akin to the addiction features we describe below. Also, to focus on hedonics does not deny
that some ascetics may have found bliss through painful self-sacrifice, but simply reflects
that positive hedonic tone is indispensable to most people seeking happiness (Bok 2010;
Bok 2010; Diener et al. 2008; Gilbert 2006; Kahneman 1999; Seligman et al. 2005).
Sensory pleasures: From sensation to ‘liking’ to hedonic feelings

First, what is pleasure? Pleasure is never merely a sensation, even for sensory pleasures
(Frijda 2010; Katz, 2006; Kringelbach 2010; Kringelbach and Berridge 2010; Ryle 1954).
Instead it always requires the recruitment of specialized pleasure-generating brain systems to
actively paint an additional “hedonic gloss” onto a sensation. Active recruitment of brain
pleasure-generating systems is what makes a pleasant experience ‘liked’.
The capacity of certain stimuli, such as a sweet taste or a loved one, to reliably elicit
pleasure – to nearly always be painted with a hedonic gloss – reflects the privileged ability
of such stimuli to activate those hedonic brain systems responsible for manufacturing and
applying the gloss. Hedonic brain systems are well-developed in the brain, spanning
subcortical and cortical levels, and are quite similar across humans and other animals.
Some might be surprised by high similarity across species, or by substantial subcortical

contributions, at least if one thinks of pleasure as uniquely human and as emerging only at
the top of the brain. The neural similarity indicates an early phylogenetic appearance of
neural circuits for pleasure and a conservation of those circuits, including deep brain
circuits, in the elaboration of later species, including humans. Substantial mechanisms for
pleasure would be selected and conserved only if they ultimately served a central role in
fulfilling Darwinian imperatives of gene proliferation via improved survival and procreation,
suggesting the capacity for pleasure must have been fundamentally important in
evolutionary fitness (Berridge and Schulkin 1989; Cabanac 2010; Darwin 1872; Nesse 2002;
Panksepp 1998; Rolls 2005; Schulkin 2004; Tindell et al. 2006).
Pleasure as an adaptive evolutionary feature is not so hard to imagine. For example, tasty
food is one of the most universal routes to pleasure, as well as an essential requirement to
survival. Not accidentally, food is also is one of the most accessible experimental methods
available to psychology and neuroscience studies of pleasure (Berridge et al. 2010; Gottfried
2010; Kringelbach 2005; Kringelbach and Berridge 2010; Peciña Smith and Berridge, 2006;
Rozin 1999; Veldhuizen et al. 2010). Much of what we will say here comes from such
studies.
Beyond food, sex is another potent and adaptive sensory pleasure which involves some of
the same brain circuits (Geogiadis and Kortekaas 2010; Komisaruk et al. 2010). Many other
special classes of stimuli also appear tap into the same limbic circuits. Even rewarding drugs
of abuse are widely viewed to hijack the same hedonic brain systems that evolved to mediate
food, sex and other natural sensory pleasures (Everitt et al. 2008; Kelley and Berridge 2002;
Koob and Volkow 2010).
Another fundamental pleasure is social interaction with conspecifics, which draws on

overlapping neural systems and is important even from an evolutionary perspective
(Aragona et al. 2006; Britton et al. 2006; Frith and Frith 2010; King-Casas et al. 2005;
Kringelbach et al. 2008; Leknes and Tracey 2008). In fact, it might well be that in humans,
at least, the social pleasures are often as pleasurable as the basic sensory pleasures.

Most uniquely, humans have many prominent higher order, abstract or cultural pleasures,
including personal achievement as well as intellectual, artistic, musical, altruistic, and
transcendent pleasures. While the neuroscience of higher pleasures is in relative infancy,
even here there seems overlap in brain circuits with more basic hedonic pleasures (Frijda
2010; Harris et al. 2009; Leknes and Tracey 2010; Salimpoor et al. 2011; Skov 2010; Vuust
and Kringelbach 2010). As such, brains may be viewed as having conserved and re-cycled
some of the same neural mechanisms of hedonic generation for higher pleasures that
originated early in evolution for simpler sensory pleasures.
Identifying pleasure generators in the brain

A state of positive affect may appear in experience to be a unitary process, but affective
neuroscience has indicated that even the simplest pleasant experience, such as a mere
sensory reward, is actually a more complex set of processes containing several
psychological components, each with distinguishable neurobiological mechanisms (Berridge
et al. 2009; Kringelbach and Berridge 2009; Leknes and Tracey 2010). These include at
least the three psychological components of wanting, liking and learning, and each has both
conscious and non-conscious sub-components. Liking is the actual pleasure component or
hedonic impact of a reward, wanting is the motivation for reward and learning includes the
associations, representations and predictions about future rewards based on past experiences.
Each of these components plays a central role in the cyclical time course of pleasure (see
Figures 1 and 2).
We distinguish between the conscious and non-conscious aspects of these sub-components

because both aspects exist in people (Winkielman et al. 2005). And at least the latter can
also be studied in other animals in ways that help reveal the underlying neural generating
mechanisms. At the potentially non-conscious level, we use quotation marks to indicate that
we are describing objective, behavioral or neural measures of these underlying brain
processes. As such, ‘liking’ reactions result from activity in identifiable brain systems that
paint hedonic value on a sensation such as sweetness. Similarly, ‘wanting’ includes
incentive salience or motivational processes within reward that mirror hedonic ‘liking’ and
make stimuli into motivationally attractive incentives, when incentive salience is attributed
to stimulus representations by mesolimbic brain systems. Finally, ‘learning’ includes a wide
range of processes linked to implicit knowledge as well as associative conditioning, such as
basic Pavlovian and instrumental associations.
At the conscious level, liking is the conscious experiences of pleasure, in the ordinary sense
of the word, which may be elaborated out of subcortical core ‘liking’ reactions by cognitive
brain mechanisms of awareness. Conscious wanting includes conscious desires for
incentives or cognitive goals, while conscious learning includes the updating of explicit and
cognitive predictions (Friston and Kiebel 2009; Zhang et al. 2009).
This conscious experience of pleasure is so striking that that pleasure has seemed purely
subjective by definition to many thinkers. But related to the notion that pleasure naturally
evolved, we maintain that pleasure also has objective aspects that can be detected in brain
and mind. Note again, however, the underlying similarities of brain mechanisms for
generating sensory pleasures in the brains of most mammals, both humans and nonhumans
alike (Figure 3). It seems unlikely so much neural machinery would have been selected and
conserved across species if it had no function. Basic pleasure reactions have always had
objective consequences, and brain mechanisms for hedonic reactions have long been
functionally useful – even before any additional mechanisms appeared that characterize any
human-unique aspects of subjective feelings of pleasure. In a sense, we suggest hedonic
reactions have been too important to survival for pleasure to be exclusively subjective. The

objective aspect has also been invaluable in identifying the brain generators of pleasure
described below.
Results
Pleasure generators: hedonic hotspots in the brain
How is pleasure actually generated within a brain? The brain appears frugal in mechanisms
that that are causally sufficient to generate ‘liking’ or magnify pleasure to high levels. These
few mechanisms are candidate brain wellsprings for hedonic happiness.
Compelling evidence for pleasure causation as increases in ‘liking’ reactions has so far been
found for activation of only a few brain substrates, or hedonic hotspots. Those hedonic
hotspots mostly reside -surprisingly, if one thought pleasure to reside primarily in the brain
cortex - deep below the neocortex in subcortical structures. Our strategy to find such neural
generators of pleasure gloss has relied on activating neural mechanisms underlying natural
‘liking’ reactions to intensely pleasant sensations. An example of ‘liking’ is the positive
affective facial expression elicited by the hedonic impact of sweet tastes in newborn human
infants (Figure 2), such as tongue protrusions that can lick the lips. By contrast, nasty bitter
tastes instead elicit facial ‘disliking’ expressions of disgust such as gapes, nose and brow
wrinkling, and shaking of the head. Many of these affective expressions are similar and
homologous in humans, orangutans, chimpanzees, monkeys, and even rats and mice (for
example, sharing features such as identical allometric timing laws in each species that scale
speed of expressions to body size) (Grill et al. 1984; Grill and Norgren 1978; Steiner 1973;
Steiner et al. 2001). Homology in origin of ‘liking’ reactions implies that the underlying
hedonic brain mechanisms are similar in humans and other animals, opening the way for an
affective neuroscience of pleasure generators that bridges both.
Subcortical hedonic hotspots in nucleus accumbens, ventral pallidum and brainstem

Some insight into pleasure-causing circuitry of human brains has been gained by affective
neuroscience studies in rodents in which the hedonic hotspots are neurochemically
stimulated to magnify a sensory pleasure, and so reveal the location and neurotransmitter
identity of the generating mechanism for intense ‘liking’. A hedonic hotspot is capable of
generating enhancements of ‘liking’ reactions to a sensory pleasure such as sweetness, when
opioid, endocannabinoid or other hedonic neurochemical receptor circuits within the hotspot
are stimulated (Mahler et al. 2007; Peciña and Berridge 2005; Peciña et al. 2006; Smith and
Berridge 2005). In rodent studies, the hotspots can be activated by painless microinjections
of drug droplets that stimulate neurotransmitter receptors on nearby neurons. Within the
hotspot, drug microinjections activate pleasure-generating systems to magnify the hedonic
impact of a sweet taste, whereas outside the border of the hotspot the same microinjections
fail to elevate ‘liking’ (thus helping to identify the location of anatomical boundaries).
The results of such studies reveal a network of several brain hedonic hotspots, distributed as
a chain of ‘liking’-enhancing islands of brain tissue across several deep structures of the
brain. The network of separate but interconnected hedonic hotspots acts together as a
coordinated whole to amplify core pleasure reactions. Activating one recruits the others as a
system (Smith et al. 2011). Each brain hotspot may be merely a cubic-millimeter or so in
volume in the rodent brain (and would be expected to be a cubic-centimeter or so in you, if
proportional to the larger human volume of whole brain). The small size of each anatomical
hotspot indicates a surprisingly localized concentration of sufficient-cause mechanisms for
generating an intense pleasure in the brain. The network properties reveal a fragile substrate
for pleasure enhancement that requires unanimity across the several parts in order to elevate
hedonic ‘liking’ (Pecina 2008; Pecina and Smith 2010; Smith et al. 2011; Smith et al. 2010).

One major hotspot has been found in the nucleus accumbens, a brain structure at the bottom
front of the brain, specifically in its medial shell region near the center of the structure.
Other hotspots have been found further back in the brain. For example, a very important
hedonic hotspot lies in the ventral pallidum, which is near the hypothalamus near the very
bottom center of the forebrain and receives most outputs from the nucleus accumbens. Still
other hotspots may be found in more distant parts of the rodent brain, possibly as far front as
limbic regions of prefrontal cortex, and almost certainly as far back as deep brainstem
regions including the parabrachial nucleus in the top of the pons (Figure 3).
Analogous to scattered islands that form a single archipelago, the network of distributed
hedonic hotspots forms a functional integrated circuit, which obeys control rules that are
largely hierarchical and organized into brain levels (Aldridge et al. 1993; Berridge and
Fentress 1986; Grill and Norgren 1978; Peciña et al. 2006). At the highest levels, the hotspot
network may function as a more democratic heterarchy, in which unanimity of positive
votes across hotspots is required in order to generate a greater pleasure. For example, any
successful enhancement that starts in one hotspot involves recruiting neuronal activation
across other hotspots simultaneously, to create a network of several that all vote ‘yes’
together for more pleasure (Smith et al. 2011). Conversely, a pleasure enhancement initiated
by opioid activation of one hotspot can be vetoed by an opposite vote of ‘no’ from another
hotspot where opioid signals are suppressed. Such findings reveal the need for unanimity
across hotspots in order for a greater pleasure to be produced, and the potential fragility of
hedonic enhancement if any hotspot defects (Smith and Berridge 2007; Smith et al. 2010).
But all of these findings on brain pleasure generators are focused on making pleasures nicer
than usual. Neurochemical activation of hedonic hotspots creates a brain wellspring for
intense pleasure when candidate sensations are encountered, generating high hedonic peaks
of sensory pleasure.
Yet well-being is a more continuous state of hedonic normalcy, in which pleasures are not
tied to any particular sensation but rather are frequent or sustained. What in the brain is
required for creating the daily continual level of a normal pleasure gloss? It turns out that
only some of the hotspots able to amplify pleasure are also necessary for maintaining normal
hedonic levels of ‘liking’ to pleasant sensations. In both the clinical literature and in our
experiments, normal core ‘liking’ reactions to pleasure are relatively difficult to abolish
absolutely by any single event, condition, brain lesion or drug (Bruno et al. 2011; Pecina
2008; Pecina and Smith 2010; Smith et al. 2010). Resilience of brain circuits for normal
baseline pleasures may be very good in evolutionary terms. Hedonic resilience may also be
related to why many people can eventually regain a reasonably happy state even after
catastrophic events (Diener et al. 2006; Gilbert 2006; Kahneman 1999). As an example,
even people in the most extreme situations, such as in suffering the near-total paralysis of
locked-in syndrome may remain happy (Bruno et al. 2011). Locked-in syndrome is a brain
condition, typically caused by a small stroke-induced lesion in the brainstem lower pons that
destroys movement pathways, which leaves the person fully aware and cognitively intact but
completely paralyzed to the extent of being able only to make slight movements of an eye or
eyelid. With an interpreter to help them pick alphabet letters one at a time, a locked-in
patient can blink or move an eye at a chosen letter to form words and communicate. Yet in
the face of even this devastating degree of paralysis, locked-in patients may often still be
happy. A recent study found that 72% of locked-in respondents did report themselves to be
moderately happy. The average response of this happy yet massively incapacitated group
was +3 out of a hedonic scale from -5 to +5, where +3 corresponded to ‘very well’ (between
+2 = ‘well’, and +4 =“almost as well at the best period in my life prior to having locked-in
syndrome”). The remaining 28% of locked-in respondents, who were much more likely to
also be experiencing pain, reported themselves to be unhappy at -4, but even this

corresponded only to “almost as bad as the worst period in my life before locked-in
syndrome” (and not quite as bad as -5 = “as bad as the worst period in my life before”); only
7% wished for euthanasia (Bruno et al. 2011). Hedonic resilience can apparently often
persist with seemingly little to go on, still generated by hedonic circuits within the person.
Those few hedonic hotspots in which damage does destroy normal pleasure might be
particularly important to hedonia in happy people. The most crucial hotspot for normal
pleasures known so far is the one in the ventral pallidum. The ventral pallidum hotspot is the
only brain location where lesion damage has been found in our lab studies to eliminate
normal sensory pleasure, and so convert sweetness from a nice into a nasty experience
(Pecina 2008; Pecina and Smith 2010; Smith et al. 2010). This site is still preserved in
locked-in patients, perhaps contributing to their remaining well-being. Damage to the ventral
pallidum brain site abolishes hedonic ‘liking’ reactions to sweetness and replaces them
instead with disgust or ‘disliking’ reactions (e.g., gapes) as though the sweet taste had turned
bitter (Berridge et al. 2010; Cromwell and Berridge 1993; Smith et al. 2010). The ventral
pallidum is the chief recipient of output from the nucleus accumbens and part of a
corticolimbic circuit that extends from prefrontal cortex to nucleus accumbens to ventral
pallidum, which then loops up via thalamus to begin the circuit all over again in prefrontal
cortex (Smith et al 2010).
An important question is how similar the ventral pallidum role in pleasure might be in
humans compared to in rodents. Currently we do not have much available data on the
hedonic consequences of human hotspot damage, because a human stroke or tumor lesion
rarely damages the ventral pallidum on both sides of the brain without also damaging
hypothalamus and related structures in between. That produces incapacitation so severe that
pleasure no longer can be specifically assessed. Yet, in a rare human case report of a brain
lesion that did rather selectively damage the ventral pallidal region on both sides without
much else, positive affect and craving for previously-addictive rewards was reported to be
much reduced (Miller et al. 2006). The patient’s brain had incurred damage to ventral
pallidum (and nearby medial globus pallidus) due to oxygen starvation when the patient
stopped breathing during an enormous drug overdose (Miller et al. 2006). Afterwards the
pallidal-lesion patient reported that his feelings became dominated by depression,
hopelessness, guilt, and anhedonia. Even formerly craved and hedonic sensations like
drinking alcohol lost their feelings of pleasure for him, and he no longer craved the many
drugs of abuse that he had previously avidly consumed. Even this lesion probably did not
fully destroy his ventral pallidum, and perhaps this is why he was not as strongly seized by
disgust as a rat would be if it had complete lesions of the ventral pallidum hotspot. Instead,
the patient still continued to eat and drink normally after his lesion, and even gained weight.
But his apparent dramatic decline in hedonic well-being suggests an impairment in normal
pleasure, and helps confirm a continuity between the ventral pallidum hotspot and human
hedonia. We have also encountered anecdotal evidence that in some patients with
pallidotomies (of nearby globus pallidus, just above and behind the human ventral pallidum)
for Parkinson’s patients, this led to severely flattened affect or anhedonia (Aziz, personal
communication). The striking restriction of brain substrates where damage converts ‘liking’
to ‘disliking’ seems a testimonial to the robustness of the brain’s capacity for a basic
pleasure reaction (Smith et al. 2010), and also perhaps an insight into what pathological
mechanisms result in true anhedonia.
Additional pleasure codes in the brain

The occurrence of pleasure is coded by neural activity in many additional forebrain sites
beyond the hotspots mentioned above, including in amygdala and in the cortex: especially
prefrontal cortical regions such as orbitofrontal cortex, anterior cingulate cortex, and insular
cortex, (Aldridge and Berridge 2010; Grabenhorst and Rolls 2011; Kringelbach 2010;

Leknes and Tracey 2010; Lundy 2008; Salimpoor et al. 2011; Skov 2010; Tindell et al.
2006; Veldhuizen et al. 2010; Vuust and Kringelbach 2010) (Figure 3).
But not all brain structures that code for pleasure actually help to cause it. Although
correlated neuroimaging activations are sometimes viewed as implying causation, there
remains a logical difference between coding and causing. Evidence indicates that the brain
often organizes these differently. Coding of pleasure in the brain can reflect not only
pleasure causation but also the neural consequences of pleasure: brain activity that results
from pleasure enhancement but causes another function, such as cognition or learning. This
implies that some brain activity may both cause and code pleasure reactions, whereas others
do not cause pleasure but may code it. Instead those other activations cause different
psychological or behavioral processes as consequences to the pleasure, such as attending to
it, learning about it, or thinking about it. Neural coding is inferred in practice by measuring
brain activity correlated to a pleasure, using techniques such as PET, fMRI and MEG
neuroimaging in humans, or electrophysiological or neurochemical activation measures in
animals presented with a rewarding stimulus (Figure 3, 4). Causation is generally inferred on
the basis of a change in pleasure caused by a brain manipulation such as lesion or
stimulation.
As a general rule, we suggest that brains operate by the principle of ‘many more codes than
causes’ for pleasure. In part, the greater number of hedonic coding sites results from the
tendency of signals to spread beyond their source, as well as from the massive need for brain
systems to translate pleasure signals into many other psychological functions, such as
learning and memory, cognitive representations, decisions, action, and consciousness.
Code-but-not-cause systems might nonetheless be reliable indicators that a pleasant event is

occurring, because they must take pleasure signals as inputs to achieve other component
processes in reward and related psychological functions. We distinguish here between the
cognitive representations and memories of reward (reward learning) and the motivational
value appraisals or decisions (reward wanting). For example, parts of the prefrontal cortex
regions sensitively code reward and hedonic impact, as described below. Yet damage to
ventromedial region of prefrontal cortex may impair the cognitive use of emotional reactions
without necessarily impairing the capacity to experience the hedonic impact of those
emotional reactions (Bechara et al. 1997; Damasio 1999; Damasio 2004; Kringelbach 2005).
The difference between coding and causing poses challenges to interpretation of brain
activations. Still, the coding of pleasure is important to identify, whether the brain activation
reflects cause or consequence. So what brain structures most specifically code pleasure?
Cortical cognition and pleasure

In humans, evidence suggests that pleasure encoding may reach an apex of cortical
localization in a subregion of orbitofrontal cortex: this hedonic-coding site is placed in the
mid-anterior and roughly mid-lateral zone of the orbitofrontal region (Figure 3, 4)
(Kringelbach 2005). In the mid-anterior zone of orbitofrontal cortex, activation revealed by
neuroimaging in people particularly correlates strongly to their subjective pleasantness
ratings of food varieties - and to other pleasures such as sexual orgasms, drugs, chocolate,
and music (Geogiadis and Kortekaas 2010; Kringelbach and Berridge 2010; Leknes and
Tracey 2010; Veldhuizen et al. 2010; Vuust and Kringelbach 2010). Most importantly,
activity in this special mid-anterior zone of orbitofrontal cortex selectively tracks changes in
subjective pleasure of a sensation even when other aspects of the same sensation remain
unchanged: such as a decline in palatability when the reward value of one food was reduced
by eating it to satiety (while pleasantness and orbitofrontal activation remained high to
another food) (Kringelbach 2005; Kringelbach et al. 2003). The mid-anterior subregion of

orbitofrontal cortex is thus a prime candidate for the coding of subjective experience of
pleasure (Kringelbach 2005).
Another potential coding site for positive hedonics in orbitofrontal cortex is a different zone
along the medial edge. The medial orbitofrontal edge has activity related to the positive
valence of affective events (Kringelbach 2010; Kringelbach and Rolls 2004), contrasted to
lateral orbitofrontal zones that have been suggested to code unpleasant events (although
lateral activity may reflect a signal to escape the situation, rather than displeasure per se)
(Kringelbach 2010; Kringelbach and Rolls 2004). This medial-lateral hedonic gradient in
orbitofrontal cortex interacts with an abstraction-concreteness gradient in the posterior-
anterior dimension, so that more complex or abstract reinforcers (such as monetary gain and
loss) are represented more anteriorly in the orbitofrontal cortex than less complex sensory
rewards that activate posterior zones (such as taste). The medial region that codes pleasant
sensations does not, however, appear to change its activity with reinforcer devaluation as
effectively as the mid-anterior subregion that best codes hedonics, and so the medial region
may not reflect the full dynamics of pleasure.
A malfunction of these hedonic mechanisms in the orbitofrontal cortex could contribute to

the profound changes in eating habits (escalating desire for sweet food coupled with reduced
satiety) that are often followed by enormous weight gain in patients with frontotemporal
dementia. This progressive neurodegenerative disorder is associated with major and
pervasive behavioral changes in personality and social conduct resembling those produced
by orbitofrontal lesions (although it should be noted that more focal lesions to the
orbitofrontal cortex have not to date been associated with obesity) (Rahman et al. 1999). It
has become clear recently that the orbitofrontal cortex also has an important role in
emotional disorders such as depression and addiction (Kringelbach 2005).
The proposed link to subjective hedonic processing might make the orbitofrontal cortex an
important gateway for neuroscientific analyses of human subjective conscious experience.
Some have even suggested that the orbitofrontal and anterior cingulate cortices together
could be viewed as part of a global workspace for access to consciousness with the specific
role of evaluating the affective valence of stimuli (Dehaene et al. 1998; Kringelbach and
Berridge 2010). In this context, it is interesting that the medial parts of the orbitofrontal are
part of a proposed network for the baseline activity of the human brain at rest (Gusnard et al.
2001), as this would place the orbitofrontal cortex as a key node in the network subserving
consciousness. This could potentially explain why all our subjective experiences have an
emotional tone and perhaps even why we have conscious pleasure.
Beyond orbitofrontal cortex, other cortical regions implicated in coding for pleasant stimuli
include parts of the mid-insular (Craig 2009) and anterior cingulate cortices (Veldhuizen et
al. 2010). As yet, however, it is not as clear as for the orbitofrontal cortex whether those
regions specifically code pleasure or only emotion more generally (Feldman Barrett and
Wager 2006). A related suggestion has emerged that the frontal left hemisphere plays a
special lateralized role in positive affect more than the right hemisphere (Davidson 2004).
Most specifically related to well-being, resting EEG activity in left prefrontal cortex has
been reported to higher in individuals with greater eudaimonic and hedonic well-being (Urry
et al. 2004). How to reconcile left-positive findings with many other findings of bilateral
activity in orbitofrontal and related cortical regions during hedonic processing remains an
ongoing puzzle.
Cortical causation of human pleasure?

Despite the evidence above for hedonic coding, however, it still remains unknown if even
the mid-anterior pleasure-coding site of orbitofrontal cortex actually causes a positive

pleasure state. It would be of considerable interest to investigate whether any of these sub-
regions of the orbitofrontal cortex are necessary or sufficient causes of pleasure, or
alternatively whether their role is restricted to cognitive elaboration of value, and translation
of hedonic affect into goal-directed plans.
One way of investigating this causation question would be to ask whether the orbitofrontal
cortex is actually required for normal pleasure reactions or conscious feelings. Only
scattered data are available, primarily from historical and case study sources. Prefrontal
lobotomies were performed on thousands of human patients in the 1950s, and may provide
some insights (Damasio 1999; Valenstein 1986). If orbitofrontal or other prefrontal areas are
necessary for basic ‘liking’ reactions, these lobotomy patients should no longer have been
able to feel pleasure. Yet perhaps surprisingly from this perspective, prefrontal lobotomy
may not produce a catastrophic loss of pleasure feelings as far as one can tell from the
available literature. Although many subtle emotional deficits occur in how patients describe
or act upon their emotions after damage to prefrontal cortex the capacity for basic ‘liking’
reactions appeared to remain intact. Lobotomy patients were by no means oblivious to the
pleasures of food, sex or other rewards.
Modern analyses of more focal prefrontal lesions report deficits in cognitive-emotional

processing of decisions of human patients, similarly do not indicate a total loss of the
capacity for pleasures (Bechara et al. 2000; Damasio 1999; Damasio 2004; Hornak et al.
2003). Decisions are often profoundly imbalanced in such patients but pleasures remain
relatively normal. Overall, mood effects of cortical lesions are mixed and generally not
hedonically devastating: although apathy and lack of affect is sometimes reported after to
the dorsomedial prefrontal cortex, the nearly opposite symptoms of euphoria, impulsiveness,
and general emotional disinhibition may be sometimes reported after damage to the
ventromedial prefrontal and orbitofrontal cortex (Tucker et al. 1995). For example, Hornak
and colleagues reported that after damage to the ventromedial prefrontal cortex and anterior
cingulate cortex, increases in emotions such as happiness and anger were reported twice as
often as decreases in emotion (typically of anger and fear when decreases occurred) (Hornak
et al. 2003). Similarly, modern patients with orbitofrontal damage hedonic manifestations of
good humor and self-satisfaction even in socially inappropriate situations, such as when
teasing a stranger (Beer et al. 2003). Thus positive hedonia does not seem abolished by
medial prefrontal or orbitofrontal cortex lesions, no matter what deficits in judgment and
decision making do result. Such considerations suggest that orbitofrontal cortex might be
more important to translating hedonic information into cognitive representations and
decisions than to generating a core ‘liking’ reaction to pleasant events (Burke et al. 2010;
Dickinson and Balleine 2010).
Similar reservations about whether pleasure is truly lost might also apply to certain types of
clinical so-called ‘anhedonia’. Anhedonia means loss of pleasure, which is often reported to
result either from disruption of cortical activity patterns in orbitofrontal, insular, and
cingulate regions of limbic cortex, or from depression or schizophrenia, or to occur
following loss of dopamine in Parkinson’s disease. Yet on closer inspection none of these
may actually entail a true loss of capacity for all pleasures; sensory pleasures especially may
persist quite intact, (Barch and Dowd 2010; Keedwell et al. 2005; Mitterschiffthaler et al.
2003; Sienkiewicz-Jarosz et al. 2005; Treadway and Zald 2011). For example, most
anhedonic patients with schizophrenia or depression still give essentially normal hedonic
ratings to the taste of sucrose (even if they have slight intensity impairments) (Berlin et al.
1998). Instead, the person retains core pleasures yet no longer seems to cognitively value
those pleasures in their life as they once did. The sub-components of pleasure means that
clinical anhedonia may be the outcome of a rather complex breakdown of cognitive
construal about underlying wanting, liking and learning processes, rather than a simple loss

of ‘liked’ pleasures themselves (Figure 5). It would be valuable to gain more information on
the pleasure capacities of patients diagnosed with clinical anhedonia.
Such evidence leads us to suggest that that the human prefrontal cortex might not actually be
needed to cause pleasure, or at least not for basic pleasures. It is possible that the main role
of the prefrontal cortex in pleasure is to act as the interface of higher order processing such
as consciousness and attention to the non-conscious pleasure generators in primarily sub-
cortical regions (Izard 2007; Kringelbach 2010; Panksepp 2007; Smith et al. 2010).
At its extreme, this position might view hedonic reactions as arising from subcortical
structures even when the subcortical brain is on its own and unable to interact with
neocortex. Some further evidence from humans, as well as much from animals, supports a
subcortical emphasis for pleasure generation. For example, Shewmon et al. described
several hydranencephalic cases in children, including a 6-year old boy with congenital
“absence of cerebral tissue rostral to the thalamus, except for small mesial temporal-lobe
remnants” and a tissue-lined cyst (p. 364), who nevertheless “smiled when spoken to and
giggled when played with. These human interactions were much more intense than, and
qualitatively different from, his positive reactions to favorite toys and music.” (p. 366)
(Shewmon et al. 1999). Similarly, Merker suggested that hydranencephalic children
“express pleasure by smiling and laughter, and aversion by “fussing,” arching of the back
and crying (in many gradations), their faces being animated by these emotional states. A
familiar adult can employ this responsiveness to build up play sequences predictably
progressing from smiling, through giggling, to laughter and great excitement on the part of
the child.”(p. 79) (Merker 2007). Such cases of emotional reaction without (hardly any)
cortex raise fascinating questions for future consideration about the relative roles of cortical
regions versus subcortical structures in human pleasures. However, no matter what
conclusion is reached regarding pleasure generation, there seems general consensus that
neocortex is crucial to link affect with complex cognition and introspection about hedonic
states.
Controversial subcortical pleasure generators? Dopamine and electrical

brain stimulation
Several other particular limbic substrates, even subcortical ones, which were once thought to
cause pleasure have now turned out not to do so after all. These include the mesolimbic
dopamine system. They also may include so-called pleasure electrodes in related brain
substrates. What is the hedonic status now of such brain substrates?
Beyond pleasure for dopamine?

Mesolimbic dopamine was long regarded as a pleasure neurotransmitter (Wise 1985), but
now is increasingly thought by many neuroscientists to fail to live up to its pleasure label.
One line of evidence against a pleasure-causing role is that mesolimbic dopamine neurons
are not always reliably activated by pleasure as such, but instead by predictive, motivational,
or attentional properties rather than hedonic properties of reward stimuli (Redgrave and
Gurney 2006; Salamone et al. 2007; Schultz et al. 1997). Another line of evidence has been
causal, such as observations that specific manipulation of dopamine either up or down
always alters motivation ‘wanting’ for rewards but often fails to shift pleasure ‘liking’
reactions to the same rewards in either animals or humans (Berridge 2007; Leyton 2010;
Smith et al. 2011). Such considerations can be combined with emerging evidence that
dopamine signals are no more necessary or sufficient causes for learning about rewards
(even if the signals often seem to code reward predictions) than for pleasure of rewards
(Berridge 2007; Flagel et al. 2010; Palmiter 2007).

Taken together, such recent findings have led to suggestions that the primary role of
mesolimbic dopamine in reward is to facilitate a psychological valuation process besides
either learning or pleasure ‘liking’. Suggestions have included motivational incentive
salience, arousal, motivation, and memory consolidation (Barbano and Cador 2007;
Berridge 2007; Niv et al. 2007; Robbins and Everitt 2007; Salamone et al. 2007). Thus the
debate continues over the role of dopamine in reward. For now, however, we think it safe to
sum up the consensus among affective neuroscientists by saying that brain mesolimbic
dopamine is not, after all, primarily a pleasure neurotransmitter.
Beyond Pleasure Electrodes?

Similarly, so-called ‘pleasure electrodes’ in the brain for 50 years were supposed to tap
directly into brain pleasure circuits (Olds 1956). However, we believe that many so-called
‘pleasure electrodes’ may actually have failed to truly cause significant pleasure at all.
Instead we suggest most electrodes more exclusively activated only the ‘wanting’
component of reward (similar to mesolimbic dopamine stimulation; which indeed is
typically activated by such electrodes). (Berridge 2003; Green et al. 2010; Kringelbach
2009; Kringelbach 2010; Kringelbach and Berridge 2010; Kringelbach et al. 2007; Smith et
al. 2010). Such electrode activations may be sought out, or may stimulate seeking of
external rewards (food, sex, gambling, shopping, etc.), yet need not be pleasant themselves.
The electrodes were originally discovered when implanted into deep brain sites that rats
would work to stimulate (Olds and Milner 1954). For example, rats readily press a lever to
stimulate brain electrodes in structures such as lateral hypothalamus, septum, nucleus
accumbens or the medial forebrain bundle that carries dopamine fibers (Olds and Milner
1954; Shizgal et al. 2001). In rats, when the same electrodes are simply turned on freely
without making the individual work for it, the electrode stimulation often also motivates the
animals to eat, drink, engage in sex, etc. (Hoebel 1988; Valenstein and Cox 1970). However,
even if electrodes make rats ‘want’ to eat food more voraciously, the same electrodes still
fail to make rats ‘like’ the food more hedonically (Berridge and Valenstein 1991). This
demonstrates dissociation between ‘wanting’ and ‘liking’ a reward, here induced by
electrode stimulation.
In humans, famous cases of intense ‘pleasure electrodes’ soon followed the original
discovery and are cited by many textbooks (Heath 1972). But when those cases are
scrutinized more closely for pleasure, we think the conclusion emerges that most electrodes
did not really cause much sensory pleasure after all, not even in the most famous cases
(Berridge 2003; Smith et al. 2010). For example, take the much cited case of “B-19”, a
young man implanted with stimulation electrodes in septum/accumbens region by Heath and
colleagues during the 1960s (Heath 1972). B-19 voraciously self-stimulated his electrode
over a thousand times in a single session, and protested when the stimulation button was
taken away. In addition, his electrode was claimed by Heath to cause “feelings of pleasure,
alertness, and warmth (goodwill); he had feelings of sexual arousal and described a
compulsion to masturbate” (p. 6, Heath 1972).
But did B-19’s electrode really cause a pleasure sensation? It is not actually so clear from
data in the reports, and B-19 was never quoted as saying it did; not even an exclamation or
anything like “Oh – that feels nice!” Instead B-19’ s electrode stimulation evoked desire to
stimulate again and strong sexual arousal - while never producing sexual orgasm or clear
evidence of actual pleasure sensation. Similarly, the stimulation never served as a substitute
for sexual acts. What it did instead was to make him want to engage in more sexual acts; just
as the stimulation made him want to press the button more.

Another example comes from a woman implanted with a deep brain electrode decades later
by a different team (Portenoy et al. 1986). Given a button box to control the electrode, she
compulsively stimulated her electrode at home: “At its most frequent, the patient self-
stimulated throughout the day, neglecting personal hygiene and family commitments” (p.
279) (Portenoy et al. 1986). When her electrode was stimulated in the clinic, it produced a
strong desire to drink liquids, and some erotic feelings, as well as a continuing desire to
stimulate again. However, “… though sexual arousal was prominent, no orgasm occurred”
(p. 279, Portenoy et al. 1986). This seems rather similar to the case of B-19: “She described
erotic sensations often intermixed with an undercurrent of anxiety. She also noted extreme
thirst, drinking copiously during the session, and alternating generalized hot and cold
sensations” (p. 282, Portenoy et al. 1986). Clearly this woman felt a mixture of subjective
feelings, but the description’s emphasis is on aversive thirst and anxiety – without evidence
of distinct pleasure sensations.
Deep brain stimulation has resurged as a therapeutic technique in the past 10 years, though
now it typically is delivered in a different way. In contemporary brain stimulation, pulses of
electrode stimulation are typically programmed by computer and delivered independently of
any action by the patient rather than requiring a patient to press a button. In many cases the
patient may not have any control at all over the stimulation pattern (though some still do).
Such programmed pulses of stimulation are being applied to pathological moods involving
depression or obsessive-compulsive disorder and to movement disorders such as Parkinson’s
disease (Green et al. 2010; Haber and Brucker 2009; Kringelbach et al. 2007; Lozano et al.
2008; Schlaepfer et al. 2007; Voon et al. 2006; Wichmann and DeLong 2006). The target
sites of such deep brain electrodes include the nucleus accumbens and the subthalamic
nucleus (Schlaepfer et al. 2008), the subgenual cingulate cortex, and fibers descending from
prefrontal cortex through the internal capsule (Lozano et al. 2008). In addition, lesions of the
posterior part of the anterior cingulate cortex have been used for the treatment of depression
with some success (Steele et al. 2008).
In some cases, the deep electrode stimulation appears helpful to the original pathological
condition, and in quite a number of instances there are positive changes in motivation or
attitude. But do such newer electrodes actually deliver pleasure or hedonic well-being? Let’s
take a closer look.
There are a few apparently promising cases for hedonic generation, at least at first glance,
but even these we think generally do not present strong evidence for pleasure on closer
scrutiny. For example, in one case, intense ‘mirthful laughter’ was generated in a man with
Parkinson’s when his subthalamic nucleus was stimulated by an electrode. The subthalamic
nucleus is connected to mesolimbic circuits of mood as well as corticostriatal circuits of
movement, and so motivational effects can accompany electrode activations intended to help
control tremor or movement problems (Krack et al. 2001). The man “initially found the
laughter amusing” (p. 869), seeming to provide a candidate for direct activation of a happier
mood state. His elevation in amusement and mood persisted while the electrode remained
on. However, it is worth noting that several doctors in the room also ‘fell into a hilaric state’
during his electrode activation though their brains received no stimulation. Laughter can be
contagious, and it might be wondered whether some of the patient’s own laughter might
have reflected something other than direct activation of a pleasurable mood of laughing
hilarity. Doubts grow further on noting what happened next: as the electrode stimulation
continued further, the man reported that “the laughter eventually became annoying and
uncomfortable”. Finally, the stimulation and laughter “became unpleasant with time and he
asked whether we could stop making him laugh” (p.870) (Krack et al. 2001). It seems his
laughter was being evoked as a complex pattern of emotional action, which could induce

either a contagious positive mood or an aversive mood that was actually unpleasant, rather
than simply reflecting a pleasantly funny state.
Another example comes from a woman with a stimulating electrode implanted in the same
subthalamic nucleus circuit: she experienced manic episodes of intense motivation when her
electrode was on. She became energized, finding herself able to do lots of things and sleep
only 3 or 4 hours at night (Herzog et al. 2003). She developed a host of new positive
affections and desires in life when her electrode was being stimulated. For example she was
described by her physicians as becoming possessed by feelings of being “in love with two
neurologists, and tried to embrace and kiss people” and engaging in binges of “unrestrained
buying of clothes” to the extent that her family wanted to take away her credit card. Yet
again, this was not a purely happy state of exhilaration even for the woman. She was also
described, while her brain was stimulated, as being “suspicious, tense and hostile. She
developed a “delusion that her sons were conspiring against her, and she said that they tried
to get her money by threat of force” (all p.1383) (Herzog et al. 2003).
Of course, our conclusion that such brain electrodes failed to cause real pleasure in these
cases does not mean that no electrode ever did, nor still less, that future pleasure electrodes
never will. One of us (MLK) has witnessed dramatic pain relief, at least, in chronic pain
patients when deep brain stimulation was turned on (Kringelbach et al. 2009), an effect
which is perhaps caused by the rebalancing of pathological oscillations in brain networks
(Kringelbach et al. 2010). Pain relief is of course important to well-being and some would
view pain relief as almost equivalent to pleasure and happiness. That view was captured for
example in William James’ slightly tongue-in-cheek quip expressed in a letter to a
correspondent after he finished a strenuous set of public lectures: “Happiness, I have lately
discovered, is no positive feeling, but a negative condition of freedom from a number of
restrictive sensations of which our organism usually seems the seat. When they are wiped
out, the clearness and cleanness of the contrast is happiness. This is why anaesthetics make
us so happy. But don’t you take to drink on that account.” (p.158) (James 1920).
Still, we believe that even William James at other moments would probably have agreed
that, however valuable relief from pain is as contrast from preceding suffering, the absence
of pain by itself is not tantamount to a positive pleasure. Absence of pain alone cannot bring
well-being or happiness. Pleasure and well-being have distinct psychological features and
require their own hedonic neural activations. And pleasure is exactly what the electrode
stimulations seem to lack as best we can tell after reviewing the available cases (Green et al.
2010; Kringelbach et al. 2007; Smith et al. 2010). At least, we surmise that the most
prototypical and classic cases of ‘pleasure electrodes’ from the past are open to grave doubt,
and most recent cases of programmed deep brain stimulation similarly seem to fail to induce
true pleasure or well-being. Continued close scrutiny of deep brain stimulation electrodes as
future studies emerge will certainly be needed to answer the question: do any electrodes
really cause pleasure?
Discussion
Incentive salience as potential explanation for dopamine and electrodes
What could such reward electrodes or mesolimbic dopamine activations be doing, if not
causing pleasure? One possible explanation is that they promote ‘wanting’ without ‘liking’.
We suggest those electrode activations and mesolimbic dopamine in general momentarily
enhance motivational value in the form of incentive salience attribution to surroundings and
stimuli perceived or imagined at that moment. The incentive salience becomes permanently
attached to those particular stimuli to make them ‘wanted’. For the original ‘pleasure
electrodes’, incentive salience would be attributed especially to the act of stimulating the

electrode via pressing the button, and to the stimuli that surround that act. If the electrodes
caused ‘wanting’, a person might well describe a sudden feeling that life was suddenly more
attractive, desirable, and compelling to pursue. If it caused ‘wanting’ attribution to the
button and the act of pressing it, people might well ‘want’ to activate their electrode again,
even if it produced no pleasure sensation. Attribution of incentive salience to nearby people
might help the individual to ‘fall in love’, and attribution to cues that are nearby or that
signify individually-favorite incentives could lead to binges of compulsive shopping,
gambling, etc. All that could be mere incentive salience ‘wanting’ – without hedonic ‘liking’
(Figure 5). It would be possible in that case to ‘want’ to press the electrode again, or to
‘want’ another incentive quite impulsively, without ever gaining significant pleasure, or
even necessarily having a clear expectation of gaining pleasure from the electrode or the
incentive target. Similar ‘wanting’ interpretations have been applied more generally to the
role of mesolimbic dopamine in reward (Berridge 2007; Berridge and Robinson 1998).
Something similar may also happen in drug addicts due to a phenomenon called drug-
induced sensitization of brain mesolimbic systems. This neural change can induce hyper-
reactivity to particular incentives, called incentive-sensitization, and may well last years.
(Robinson and Berridge 1993; Robinson and Berridge 2003). Considerable evidence has
recently emerged to bear on such excesses of desire (Boileau et al. 2006; Camerer 2006;
Evans et al. 2006; Finlayson et al. 2007; Lawrence et al. 2003; Leyton 2010; Robinson and
Berridge 2003; Wiers et al. 2007; Wiers and Stacy 2006).
Bridging pleasure to meaning

It is interesting to note that all brain structures discussed above or being targeted for brain-
based treatments of pathological mood disorders today either have close links with the
hedonic network we have considered (e.g., orbitofrontal cortex, nucleus accumbens and
ventral pallidum, etc.) or belong to what has been termed the brain’s default network which
changes over early development (e.g., additional regions of prefrontal cortex, or of cingulate
cortex, temporal cortex, and parietal cortex) (Fair et al. 2008; Fransson et al. 2007) (Figure
4).
Mention of the default network brings us back to the topic of eudaimonic happiness, and to
potential interactions of hedonic brain circuits with circuits that assess meaningful
relationships of self to social others. The default network is a steady state circuit of the brain
which becomes perturbed during cognitive tasks (Gusnard et al. 2001). Most pertinent here
is an emerging literature that has proposed the default network to carry representations of
self (Lou et al. 1999), internal modes of cognition (Buckner et al. 2008), and perhaps even
states of consciousness (Laureys et al. 2004). Such functions might well be important to
higher pleasures as well as meaningful aspects of happiness.
Although highly speculative, we wonder whether the default network might deserve further
consideration for a role in connecting eudaimonic and hedonic happiness. At least, key
regions of the frontal default network overlap with the hedonic network discussed above,
such as the anterior cingulate and orbitofrontal cortices (Beckmann et al. 2009; Kringelbach
and Rolls 2004; Steele et al. 2008), and have a relatively high density of opiate receptors
(Henriksen and Willoch 2008). Eudaimonic wellbeing may be correlated with activity in the
anterior cingulate and in left prefrontal cortex, perhaps though the ability to suppress
negative emotions (Urry et al. 2004; Urry et al. 2006; van Reekum et al. 2007). Activity
changes in the frontal default network, such as in the subgenual cingulate and orbitofrontal
cortices, correlate to pathological changes in subjective hedonic experience, such as in
depressed patients (Davidson et al. 2002).

Pathological self-representations by the frontal default network could also provide a

potential link between hedonic distortions of happiness that are accompanied by eudaimonic
dissatisfaction, such as in cognitive rumination of depression (Addis et al. 2007; Gusnard et
al. 2001; Schacter et al. 2007; Schnider 2003). Conversely, mindfulness-based cognitive
therapy for depression, which aims to disengage from dysphoria-activated depressogenic
thinking might conceivably recruit default network circuitry to help mediate improvement in
happiness via a linkage to hedonic circuitry (Teasdale et al. 2000).
Beyond the default network, other cortical networks have been proposed to correspond by
direct activation with eudaimonic evaluations of self, relation to others, and with meaningful
themes related to life satisfaction (Heller et al. 2009; Schacter et al. 2007). These include
dorsolateral prefrontal, and other parietal and temporal cortex networks. In short, the default
network and lateral cortical networks whose activation encodes evaluations of self and life
meaning stand among the brain candidates for a substrate that might mediate eudaimonic
appraisals. How these networks actually embody eudaimonia components, and how they
link evaluations of life meaningfulness and satisfaction with pleasurable states of hedonia,
remains a major puzzle for psychological neuroscience to unravel in the future.
Conclusions
While some progress has been made in understanding brain hedonics, it is important not to
over-interpret. We do not yet have a neuroscience of happiness. We have merely aimed to

sketch out the beginnings of a hedonic approach that may prove fruitful. Further, when all is
done, one may still question our entire effort, based as it is largely on evidence from sensory
pleasures. Some will demur that pleasure, our chief focus here, is irrelevant after all to true
happiness. For many, this view might be well expressed by the words of John Stuart Mill, “It
is better to be a human being dissatisfied than a pig satisfied; better to be Socrates
dissatisfied than a fool satisfied.” (Mill, Crisp and NetLibrary Inc. 1998)(p. 57). By the view
expressed in this quotation, a life filled with the most intense pleasures of pigs or fools
would never be enough for happiness because true happiness hinges on a superior kind of
psychological or eudaimonic richness that is unique to the enlightened, though hedonically
dissatisfied, Socrates (Mill himself, however, seemed to assent elsewhere that hedonic
pleasure was important to happiness too).
At the opposite extreme, Sigmund Freud seemed to take a purely hedonic view of happiness,
more likely to favor our endeavor. Freud wrote, in response to his own question concerning
what people demand of life and wish to achieve in it, the reply “The answer to this can
hardly be in doubt. They strive after happiness; they want to become happy and to remain
so. This endeavor has two sides, a positive and a negative aim. It aims, on the one hand, at
an absence of pain and displeasure, and, on the other, at the experiencing of strong feelings
of pleasure” (Freud 1930)(p.76). Freud’s answer equates hedonic pleasure with happiness.
According to this view, the more pleasure you have (while avoiding displeasure), the
happier you are. Modern psychologists tend to fall in between these poles. Yet relatively few
today would deny that hedonic pleasure is at least relevant to a final state of well-being.
We do not pretend to see deeper into the nature of happiness than those thinkers of earlier
times, but simply point again to the empirical convergence of hedonic and eudaimonic
features together in most people who are actually happy. And we note in conclusion, that so
far as positive affect contributes to happiness, then at least some progress has been made in
understanding the neurobiology of pleasure in ways that might be relevant.
In finishing, we can imagine several possibilities to relate happiness to particular hedonic

psychological processes discussed above. Thus, one way to conceive of hedonic happiness is

as ‘liking’ without ‘wanting. That is, a state of pleasure without disruptive desires, a state of
contentment (Kringelbach and Berridge 2009). A different possibility is that moderate
‘wanting’, matched to positive ‘liking’, facilitates engagement with the world. A little
incentive salience may add zest to the perception of life and perhaps even promote the
construction of meaning, just as in some patients therapeutic deep brain stimulation may
help lift the veil of depression by making life events more appealing. However, too much
‘wanting’ can readily spiral into maladaptive patterns such as addiction, and is a direct route
to great unhappiness. Finally, all might agree that happiness springs not from any single
component but from the interplay of higher pleasures, positive appraisals of life meaning
and social connectedness, all combined and merged by interaction between the brain’s
default networks and pleasure networks. Achieving the right hedonic balance in such ways
may be key to the brain’s generation of positive well-being.
Acknowledgments
The authors’ research has been supported by grants from the NIH (MH63644 and DA015188) to KCB, and from
the TrygFonden Charitable Foundation, Braveheart Charity, Novo Nordisk Foundation to MLK. We thank Asma’u
Mustapha and two anonymous reviewers for helpful comments on an earlier version of the manuscript. This essay
was modified from recent articles by the authors.
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Figure 1. Pleasure cycles

One way to view the difference between pleasure ‘liking’ and other components of reward is
as cyclical time course common to many everyday moments of positive affect. Typically,
rewarding moments go through a phase of expectation or wanting for a reward, which
sometimes leads to a phase of consummation or liking with the reward that can have a peak
level of pleasure (e.g. encountering a loved one, a tasty meal, sexual orgasm, drug rush,
winning a gambling bet). This can be followed by a satiety or learning phase, where one
learns and update our predictions for the reward. These various phases have been identified
at many levels of investigation of which the recent research on the computational
mechanisms underlying prediction, evaluation and prediction error are particularly
interesting (Friston and Kiebel 2009; Zhang et al. 2009). Note, however, that some rewards
might possibly lack a satiety phase (suggested candidates for brief or missing satiety phase
have included money, some abstract rewards and some drug and brain stimulation rewards
that activate dopamine systems rather directly).

Figure 2. Measuring reward and hedonia

Hedonic reward processes related to well-being involve multifaceted psychological
components. Major processes within reward (first column) consist of wanting or incentive
salience (white), learning (blue), and - most relevant to happiness - pleasure liking or
hedonic impact (light blue). Each of these contains explicit (top rows, light yellow) and
implicit (bottom rows, yellow) psychological components (second column) that constantly
interact and require careful scientific analysis to tease apart. Explicit processes are
consciously experienced (e.g. explicit pleasure and happiness, desire, or expectation),
whereas implicit levels of the same psychological processes are potentially unconscious in
the sense that they can operate at a level not always directly accessible to conscious
experience (implicit incentive salience, habits and ‘liking’ reactions), and must be further
translated by other mechanisms into subjective feelings. Measurements or behavioral
procedures that are especially sensitive markers of the each of the processes are listed (third
column).

Figure 3. Hedonic brain circuitry

The schematic figure shows the brain regions for causing and coding fundamental pleasures
in rodents and humans. (a) Facial ‘liking’ and ‘disliking’ expressions elicited by sweet and
bitter taste are similar in rodents and human infants. (b, d) Pleasure causation has been
identified in rodents as arising from interlinked subcortical hedonic hotspots, such as in
nucleus accumbens and ventral pallidum, where neural activation may increase ‘liking’
expressions to sweetness. Similar pleasure coding and incentive salience networks have also
been identified in humans. (c) We believe the so-called ‘pleasure’ electrodes in rodents and
humans were unlikely to have elicited much true pleasure but perhaps only incentive
salience or ‘wanting’. (d) The cortical localization of pleasure coding may reach an apex in
various regions of the orbitofrontal cortex, which differentiate subjective pleasantness from
valence processing of aspects the same stimulus, such as a pleasant food.

Figure 4. The brain’s default network and eudaimonic - hedonic interaction

(a - c) The brain’s default network has been linked to self-awareness, remembering the past
and prospecting the future (Addis et al. 2007; Gusnard et al. 2001; Schacter et al. 2007).
Some components overlap with pleasure networks, including midline structures such as the
orbitofrontal, medial prefrontal and cingulate cortices. We wonder whether happiness might
include a role for the default network, or for related neural circuits that contribute to
computing relations between self and others, in evaluating eudaimonic meaning and
interacting with hedonic circuits of positive affect. Examples show key regions of the
default network such as (d) the anterior cingulate and orbitofrontal cortices that have a high
density of opiate receptors (Willoch et al. 2004), (e) have been linked to depression (Drevets
et al. 1997), and (f) its surgical treatment. (g) have been implicated by connectivity analyses
(Beckmann et al. 2009), (h) are implicated in pleasure-related cognitive functions such as
monitoring, learning and memory (Kringelbach 2005), (i) or in self-knowledge, person
perception and other cognitive functions (Amodio and Frith 2006). (j) The default network
may change over early life in infants and children (Fair et al. 2008; Fransson et al. 2007), (k)
in pathological states including depression and vegetative states (Laureys et al. 2004), (l)
and after cortical lesions that disrupt reality monitoring and create spontaneous
confabulations (Schnider 2003).

Figure 5. Balancing and unbalancing of the pleasure processes in the brain

In the normal brain, wanting, liking, and learning processes are balanced over time (column
1). The breakdown of the balance between these processes can lead on the one hand to
anhedonia (the lack of pleasure ‘liking’), or of avolition and apathy (the lack of incentive
salience ‘wanting’). On the other hand, an opposite imbalance can lead to addiction or
related impulsive-compulsive motivation disorders (excessive incentive salience ‘wanting’).
The above depicts a progressive decrease in both wanting and liking (column 2) which is
markedly different from an addictive increase in wanting, which can induce excessive
motivation even if there is a decrease in liking (column 3). This has been proposed to be the
case in addiction (Robinson and Berridge 1993).

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Psychol Well Being. 2011 October 24; 1(1): 1–3. doi:10.1186/2211-1522-1-3.

Building a neuroscience of pleasure and well-being

2Department of Psychiatry, Warneford Hospital, University of Oxford, Oxford, UK

brain systems relevant to self-understanding and the meaning components of eudaimonic

© 2011 Berridge and Kringelbach; licensee Springer.

neuroscience is to understand how pleasure is generated by brain mechanisms so as to

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

Sensory pleasures: From sensation to ‘liking’ to hedonic feelings

Some might be surprised by high similarity across species, or by substantial subcortical

Another fundamental pleasure is social interaction with conspecifics, which draws on

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

Identifying pleasure generators in the brain

Figures 1 and 2).

We distinguish between the conscious and non-conscious aspects of these sub-components

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

Subcortical hedonic hotspots in nucleus accumbens, ventral pallidum and brainstem

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

Additional pleasure codes in the brain

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

Code-but-not-cause systems might nonetheless be reliable indicators that a pleasant event is

Cortical cognition and pleasure

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

A malfunction of these hedonic mechanisms in the orbitofrontal cortex could contribute to

Cortical causation of human pleasure?

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

of hedonic affect into goal-directed plans.

Modern analyses of more focal prefrontal lesions report deficits in cognitive-emotional

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

Controversial subcortical pleasure generators? Dopamine and electrical

Beyond pleasure for dopamine?

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

Beyond Pleasure Electrodes?

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

Bridging pleasure to meaning

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

Pathological self-representations by the frontal default network could also provide a

over-interpret. We do not yet have a neuroscience of happiness. We have merely aimed to

In finishing, we can imagine several possibilities to relate happiness to particular hedonic

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

Psychol Well Being. Author manuscript; available in PMC 2012 February 8.

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