![]() Orexin signals from the lateral hypothalamic modulate mesocorticolimbic activity by integrating circulating signals about hunger/satiety in order to enhance or suppress ‘liking’ and incentive motivation during various physiological states. Brain hedonic hotspots (shown in orange) and coldspots (shown in light blue) in parabrachial nucleus, ventral pallidum, nucleus accumbens, orbitofrontal cortex, and insula do not share direct projections. Adapted from Castro & Berridge (2014).Ī) Top panel shows a sagittal view of a rat brain with a summary map of connections between hindbrain, hypothalamic, and mesocorticolimbic sites that mediate ‘liking’, ‘wanting’, sensory signals, and appetite. Finally, kappa opioid stimulation did not reliably generate feeding at any site despite generating intense ‘liking’ expressions in the rostrodorsal quadrant. By comparison, delta opioids generate feeding within anterior sites overlapping with the hedonic hotspots. Mu-opioid agonists generated feeding throughout the entire medial shell. Bottom panels shows the dissociable effects of mu, delta, and kappa manipulations in the nucleus accumbens medial shell on free-feeding. While microinjections into anterior dorsal (in red) sites magnified ‘liking’ expressions to sucrose solutions, posterior manipulations oppositely suppress ‘liking’ expressions (in blue). Similar patterns of hedonic enhancements were found after mu, delta, and kappa opioid agonists. B) Bottom-top panel shows dissociations between ‘liking’ and ‘wanting’ in the nucleus accumbens medial shell following microinjections of mu-opioid agonists (DAMGO), delta-opioid agonists (DPDPE), and kappa-opioid agonists (U50488H). DNQX or muscimol in mid NAc medial shell produce a mix of appetitive and aversive motivations. The same microinjections at posterior sites generate fearful motivations (depicted in red) such as distress calls, bites, escape attempts, and defensive treading. ![]() Manipulations into anterior sites produce voracious feeding (shown in green). By comparison, the same manipulations within the hedonic coldspots (pictured in blue) oppositely suppress ‘liking’ reactions to sucrose solutions.Ī) Top shows amino acid disruptions (via glutamate AMPA receptor antagonist DNQX or GABA A agonist muscimol) in the medial shell of the nucleus accumbens reveal a rostral to caudal organization of intense motivations. ‘Liking’ is mediated by hedonic hotspots (pictured in red) where opioid, orexin, endocannabinoid, and optogenetic manipulations enhance positive orofacial expressions to sucrose taste. ‘Wanting’ is generated by mesolimbic dopamine systems originating from the midbrain that project to various limbic structures (pictured in green) to generate incentive salience. Sagittal view of a rat brain depicting brain systems of ‘wanting’ and ‘liking’. B) Palatable foods and their predictive cues activate mesocorticolimbic reward systems. Orofacial expressions to palatable and aversive solutions are homologous across various mammalian species that include human infants, nonhuman primates, rodents, and horses. Negative aversive orofacial expressions (‘disgust’) in response to bitter quinine solutions (right). All rights reserved.Ī) Positive hedonic expressions (‘liking’) elicited in response to palatable sucrose solutions (left). ![]() Future findings on the neurobiological bases of 'liking' and 'wanting' can continue to improve understanding of both normal food reward and causes of clinical eating disorders.įeeding Nucleus accumbens Prefrontal cortex Ventral pallidum ‘Liking’ ‘Wanting’.Ĭopyright © 2020 Elsevier Inc. Emerging evidence suggests that some cases of obesity and binge eating disorders may reflect an incentive-sensitization brain signature of cue hyper-reactivity, causing excessive 'wanting' to eat. Via incentive sensitization, 'wanting' selectively becomes higher, especially when triggered by reward cues when encountered in vulnerable states of stress, etc. In some conditions such as drug addiction, 'wanting' is known to dramatically detach from 'liking' for the same reward, and this may also occur in over-eating disorders. Hedonic and motivational circuitry interact together and with hypothalamic homeostatic circuitry, allowing relevant physiological hunger and satiety states to modulate 'liking' and 'wanting' for food rewards. In turn, a much larger mesocorticolimbic circuitry generates 'wanting' or incentive motivation to obtain and consume food rewards. Hedonic hotspots are found in nucleus accumbens medial shell, ventral pallidum, orbitofrontal cortex, insula cortex, and brainstem. Mesocorticolimbic mechanisms that enhance 'liking' include brain hedonic hotspots, which are specialized subregions that are uniquely able to causally amplify the hedonic impact of palatable tastes. It is becoming clearer how neurobiological mechanisms generate 'liking' and 'wanting' components of food reward.
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