'Liking' and 'wanting' in eating and food reward: Brain mechanisms and clinical implications

Abstract

It is becoming clearer how neurobiological mechanisms generate 'liking' and 'wanting' components of food reward. 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. Hedonic hotspots are found in nucleus accumbens medial shell, ventral pallidum, orbitofrontal cortex, insula cortex, and brainstem. In turn, a much larger mesocorticolimbic circuitry generates 'wanting' or incentive motivation to obtain and consume food rewards. 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 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. Via incentive sensitization, 'wanting' selectively becomes higher, especially when triggered by reward cues when encountered in vulnerable states of stress, etc. 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. 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.

Keywords: Feeding; Nucleus accumbens; Prefrontal cortex; Ventral pallidum; ‘Liking’; ‘Wanting’.

Fig. 1.. Brain systems of ‘wanting’ and ‘liking’.

A) Positive hedonic expressions (‘liking’) elicited in response to palatable sucrose solutions (left). Negative aversive orofacial expressions (‘disgust’) in response to bitter quinine solutions (right). Orofacial expressions to palatable and aversive solutions are homologous across various mammalian species that include human infants, nonhuman primates, rodents, and horses. B) Palatable foods and their predictive cues activate mesocorticolimbic reward systems. Sagittal view of a rat brain depicting brain systems of ‘wanting’ and ‘liking’. ‘Wanting’ is generated by mesolimbic dopamine systems originating from the midbrain that project to various limbic structures (pictured in green) to generate incentive salience. ‘Liking’ is mediated by hedonic hotspots (pictured in red) where opioid, orexin, endocannabinoid, and optogenetic manipulations enhance positive orofacial expressions to sucrose taste. By comparison, the same manipulations within the hedonic coldspots (pictured in blue) oppositely suppress ‘liking’ reactions to sucrose solutions.

Fig. 2.. ‘Liking’, ‘wanting’, desire, and dread in the nucleus accumbens medal shell.

A) 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. Manipulations into anterior sites produce voracious feeding (shown in green). The same microinjections at posterior sites generate fearful motivations (depicted in red) such as distress calls, bites, escape attempts, and defensive treading. DNQX or muscimol in mid NAc medial shell produce a mix of appetitive and aversive motivations. 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). Similar patterns of hedonic enhancements were found after mu, delta, and kappa opioid agonists. While microinjections into anterior dorsal (in red) sites magnified ‘liking’ expressions to sucrose solutions, posterior manipulations oppositely suppress ‘liking’ expressions (in blue). Bottom panels shows the dissociable effects of mu, delta, and kappa manipulations in the nucleus accumbens medial shell on free-feeding. Mu-opioid agonists generated feeding throughout the entire medial shell. By comparison, delta opioids generate feeding within anterior sites overlapping with the hedonic hotspots. Finally, kappa opioid stimulation did not reliably generate feeding at any site despite generating intense ‘liking’ expressions in the rostrodorsal quadrant. Adapted from Castro & Berridge (2014).

Fig. 3.. The posterior ventral pallidum is necessary for normal hedonic function.

Microinjections of mu-opioid and orexin agonists (left) into the pallidum revealed a rostral to caudal organization of hedonic function. Stimulation of the posterior ventral pallidum ‘hotspot’ causally amplifies sucrose orofacial expressions (‘liking’) while the same manipulations in the caudal hedonic ‘coldspot’ suppress them. Temporary inactivation of posterior VP via GABA agonists generates a reversal of hedonic function so that normally ‘liked’ sucrose solutions elicit aversive ‘disgust’ reactions. Adapted from Smith & Berridge (2005) and Ho & Berridge (2014).

Fig. 4.. Brain Systems for Appetite and Motivation.

A) 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. 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. 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. Additional hypothalamic systems in the arcuate nucleus of the hypothalamus may interact with mesolimbic circuitry so that their activity reflects the incentive value of food and food-related cues in the environment. Colors of arrows denote projection types. Data is based from studies described in text. B) Bottom panel is a sagittal view of mesocorticolimbic systems that mediate ‘liking’ and ‘wanting’ in humans. Individuals with eating disorders may have hyper-reactive mesolimbic dopamine systems that respond to information about food and their related cues in the environment. This enhanced dopamine release may assign excessive incentive salience that results in overconsumption of palatable foods that is independent of how much those foods are actually ‘liked’.