Research Projects
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Hedonic hotspots of 'Liking' -- The brain's pleasure gloss

Pleasure arises within the brain. Sweetness or other natural pleasures are mere sensations as they enter the brain, and brain systems must actively paint the pleasure onto sensation to generate a 'liking' reaction -- as a sort of pleasure gloss or varnish. Our lab has discovered several 'hedonic hotspots' in the brain that paint pleasure on sensation. A hedonic hotspot is a brain site with a concentration of pleasure-causing mechanisms. It is all the more urgent to identify true hedonic hotspots now because several brain candidates traditionally thought to mediate pleasure are increasingly recognized to not be pleasure mechanisms after all (e.g., dopamine, electrical brain stimulation). [General review papers on pleasure 'liking':. Affective neuroscience of pleasure 2008Hedonic hotspots]

The hedonic hotspots that generate pleasure 'liking' are each about a cubic millimeter in size (in rats; perhaps a cubic centimeter in you), and contained in limbic forebrain structures such as the nucleus accumbens and the ventral pallidum. In hotspots the hedonic gloss that amplifies natural pleasure is painted by brain chemicals such as mu opioids and endocannabinoids, which are natural brain versions of heroin and marijuana. If we activate those neurochemical receptors (via painless microinjection of tiny droplets of drug directly into a hedonic hotspot) we increase the 'liking' reactions elicited by sweetness. [Research examples]

We have developed a Fos plume microinjection mapping technique to precisely map the hedonic hotspots (and chemical pleasure paints) that amplify 'liking'. We have also studied how pleasure is coded by the firing patterns of neurons within those hotspots, similar to a brain Morse code for 'liking', in collaboration with the Aldridge lab. Our goal is to better understand how brain hedonic hotspots act together in an integrated hedonic circuit to mediate 'liking' for sensory pleasures Hedonic hotspots.

What is 'liking'? 'Liking' is an objective process of positive hedonic reaction that underlies subjective sensory pleasure. We rely on a useful natural window into 'liking' reactions, facial affective expressions of taste pleasure ['liking' expressions that are homologous in human infant, non-human primates, and even rodents[Infant/primate sample; Expression overview)]. Combining that window into 'liking' with painless neuroscience techniques, we map the brain hedonic hotspots that paint a pleasure gloss onto sensation [Pleasure overviewsAffective neuroscience of pleasure 2008].

Hedonic hotspots in Nucleus accumbens and in Ventral Pallidum hedonic hotspots

Side view of hedonic hotspot in nucleus accumbens where opioids amplify sweetness 'liking' (red/yellow) based on Peciña & Berridge (2005).

Three views of hedonic hotspot in ventral pallidum where opioids amplify 'liking' (red) based on Smith & Berridge (2005).

What's a ventral pallidum? The limbic ventral pallidum is relatively new on the affective neuroscience scene, having been named by anatomists only a decade or so ago. It lies at the base of the forebrain, in front of the hypothalamus, and as chief target of nucleus accumbens is the output channel through which most mesocorticolimbic circuits must work. . We have found a special hedonic hotspot that is crucial for reward ‘liking’ and ‘wanting’ (and codes reward learning too). The opioid hedonic hotspot is shown in red above. It works together with another hedonic hotspot in the more famous nucleus accumbens to generate pleasure 'liking'.


'Wanting' - Incentive Salience
How does reward 'wanting' differ from reward 'liking'? A common brain myth is that dopamine mediates sensory pleasure, but our research has helped indicate that dopamine mediates only a form of ''wanting' for reward called incentive salience, and not pleasure 'liking'. Our goal is to better understand the psychological nature of incentive salience and to clarify its brain mesolimbic mechanisms. To study neural substrates of 'wanting', we use psychological and neurobiological techniques that isolate incentive salience from other psychological functions such as reinforcement learning or pleasure 'liking'. Our measures inclued cue-triggered 'wanting' ( based on Pavlovian-instrumental transfe), and 'motivational magnet' features of reward cues ( based on autoshaping). Some of our studies involve collaboration on hyperdopaminergic DAT-knockdown mutant mice (with Xiaoxi Zhuang at U. Chicago), and on limbic neuronal coding (with J. Wayne Aldridge ). Sensitization of 'wanting' may be an important component of addiction .

(Mutant Mice sample; 'Wanting' overview 1 ; 'Wanting' overview 2 ).


Desire versus dread in in limbic nucleus accumbens
What determines if something is nice or nasty? Does desire share anything in common with fear? We have found neural affective building blocks that generate both desire and dread, embedded in a limbic keyboard or brain map of affective valence (positive versus negative emotion organinzed in rostrocaudal gradients) in the nucleus accumbens Flipping desire vs dread. Affective building blocks may also include hidden incentive components inside stress, such as CRF mechanisms that act in nucleus accumbens to amplify incentive 'wanting'. This may contribute to the ability of stress to precipitate binges of compulsive consumption.. See a natural 'rodent dread' behavior exploited by our affective neuroscience studies (antipredator defensive burying):



Addiction
Why is drug addiction so compulsive and long lasting? The distinction of 'wanting' from 'liking' has important implications found in the Incentive-Sensitization theory of addiction
. Addictive drugs can cause permanent neural sensitization in brain mesolimbic systems of incentive salience. Sensitized incentive salience means addicts have compulsive 'wanting' to take drugs, which can last months or years. Much evidence has emerged to favor this idea in the decade since Terry Robinson and Berridge first proposed it, and it continues to influence current neuroscience research . We stress Incentive-Sensitization theory does not provide a cure for addiction, but it does help pinpoint a crucial aspect of what goes wrong. That understanding may eventually aid design of a more adequate cure. Our lab is now working to better understand exactly how drug-induced neural sensitization distorts psychological and neurobiological mechanisms of ‘wanting’ and ‘liking’ to produce addiction (Incentive sensitization research sample ).
Other Human Applications
Incentive salience 'wanting' mechanisms have implications for other forms of human irrational desire (Irrational choices
). We are also exploring how basic 'liking' / 'wanting' systems may relate to conscious and unconscious emotion processes in normal people (Unconscious emotion; see also Piotr Winkielman's web page).