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 brain generators of sensory pleasure as a system of anatomical ‘hedonic hotspots’ in the brain, which can paint intense pleasure on sensation. This helps to identify true mechanisms of pleasure in the brain. This is all the more important because several other brain candidates once thought to mediate pleasure turn out to not cause pleasure after all on closer inspection (e.g., dopamine, electrical brain stimulation). Understanding how the brain truly causes pleasure has important implications for unraveling how hedonic dysfunctions cause mood disorders, drug addiction and related clinical disorders [General review papers on pleasure ‘liking’: (PDF) (PDF)
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, the ventral pallidum, and limbic regions of prefrontal cortex. In hotspots the hedonic gloss is painted by brain chemicals such as mu opioids and endocannabinoids, which are natural brain versions of heroin and marijuana that amplify a sensory pleasure. If we activate neural hotspot mechanisms (by painlessoptogenetic laser stimulations or microinjection of tiny droplets of drug directly into a hedonic hotspot) we can double or triple ‘liking’ reactions to a sensory pleasure. [Research examples]
Using lasers or microinjections to activate the brain (PDF) (PDF). We have developed a Fos plume mapping technique to more precisely map the hedonic hotspots revealed by optogenetic laser stimulations or by drug microinjections that amplify ‘liking’. . In optogenetic stimulation, we use laser pulses of light to activate particular neurons, which have been targeted by a virus microinjection carrying a gene that makes infected neurons develop photoreceptors and become activated by light (photo of brain illuminated by optic fiber that transmits laser). (PDF)
Our goal is to better understand how brain hedonic hotspots act together in an integrated hedonic circuit to mediate ‘liking’ for sensory pleasures. Overview from Intelligent Life.
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 (PDF); Pleasure ‘liking; overview) (PDF)].Combining that window into ‘liking’ with painless neuroscience techniques, we map the brain hedonic hotspots that paint a pleasure gloss onto sensation [Pleasure overviews] (PDF) (PDF) (PDF).
Hedonic hotspots in Nucleus accumbens and in Ventral Pallidum
LEFT: ‘ Liking’ and ‘disliking’ expressions to taste in human, orangutan and rat. Brain map showing pleasure site in accumbens where opioid neurotransmission causes sweetness ‘liking’. Bars show morphine microinjections increase ‘liking’ reactions.
RIGHT: Fearful defensive treading displayed by ground squirrel and rat to threats (rattlesnake or shockprod). Brain map (side view) shows gradient of desire versus dread in nucleus accumbens, where microinjections cause either feeding or fearful treading. Bars show fearful defensive treading caused especially by posterior microinjections.
Description of pictures from Kelley & Berridge, Neuroscience of natural rewards, Journal of Neuroscience (2002).
Three views of hedonic hotspot in ventral pallidum where opioids and orexin amplify ‘liking’ (red) based on Smith & Berridge (2005) and Ho & Berridge (2013; 2014).
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’. PDF
‘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. We are currently studying how brain circuits converge current motivation with prior learning to focus ‘wanting’ on particular targets, relevant to why addicts ‘want’ mostly drugs whereas binge eaters ‘want’ mostly food. (PDF) (PDF)
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 brain manipulations include optogenetic laser activations to stimulate ‘wanting’ systems (PDF). Our measures include cue-triggered ‘wanting’ ( based on Pavlovian-instrumental transfer), and ‘motivational magnet’ features of reward cues ( based on autoshaping). Sensitization of ‘wanting’ may be an important component of irrational desires such as addiction. (PDF) (PDF).
(; ‘Wanting’ overview 1 ).
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 organized in rostrocaudal gradients) in the nucleus accumbens. (PDF) Affective building blocks may also include hidden incentive components inside stress, such as CRF mechanisms that act in nucleus accumbens to amplify incentive ‘wanting’. (PDF) 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):
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.
Other Human Applications
Incentive salience ‘wanting’ mechanisms have implications for other forms of human irrational desire (Irrational choices). (PDF) We have also explored how basic ‘liking’ / ‘wanting’ systems may relate to conscious and unconscious emotion processes in normal people (Unconscious emotion; (PDF) see also Piotr Winkielman’s web page).