Dissecting components of reward: 'liking', 'wanting', and learning

Abstract

In recent years significant progress has been made delineating the psychological components of reward and their underlying neural mechanisms. Here we briefly highlight findings on three dissociable psychological components of reward: 'liking' (hedonic impact), 'wanting' (incentive salience), and learning (predictive associations and cognitions). A better understanding of the components of reward, and their neurobiological substrates, may help in devising improved treatments for disorders of mood and motivation, ranging from depression to eating disorders, drug addiction, and related compulsive pursuits of rewards.

Figure 1

Example behavioral ‘liking’ reactions and brain hedonic hotspots for a sensory pleasure. Top: Positive hedonic ‘liking’ reactions are elicited by sucrose taste from human infant and adult rat (e.g. rhythmic tongue protrusion). By contrast, negative aversive ‘disliking’ reactions are elicited by bitter quinine taste. Below: Forebrain hedonic hotspots in nucleus accumbens shell and in ventral pallidum where mu opioid agonist microinjections cause amplification of ‘liking’ reactions to sweetness. Red/yellow indicates greatest amplification of ‘liking’ for the sensory pleasure. Modified based on data from [14••,17•,28].

Figure 2

Expansion of mu opioid hotspot in nucleus accumbens with delineation of ‘liking’ versus ‘wanting’ zones. Green: the entire medial shell mediates opioid-stimulated increases in ‘wanting’ for food reward. Orange-red: circumscribed cubic-millimeter sized hedonic hotspot generates increases in ‘liking’ after the same opioid stimulation. Blue: a small hedonic ‘coldspot’ suppresses ‘liking’ reactions to sucrose, whereas a larger purple zone suppresses ‘disliking’ reactions to quinine. Reprinted with permission from [27], based on data from [14••].

Figure 3

Neuronal coding of ‘liking’ for the sensory pleasure of sweet and salty tastes. Neuronal firing responses are shown from a ventral pallidum recording electrode to tastes of sucrose and intense salt infused into the mouth of a rat. Two conditions were tested for both tastes: a baseline condition of normal physiological balance (in which intense salt is ‘disliked’ and sugar is ‘liked’), and a depletion condition of sodium deficit and salt appetite (in which both tastes are ‘liked’). Time = 0 is when each taste infusion began. Modified from [7••].

Figure 4

NAc amphetamine amplification of cue-triggered ‘wanting.’ Transient peaks of ‘wanting’ for sucrose reward are triggered by 30-s appearances of a Pavlovian sucrose cue in a Pavlovian-Instrumental Transfer test (CS+; right). Amphetamine microinjection in nucleus accumbens magnifies ‘wanting’ for sugar reward — only in the presence of the reward cue (CS+), indicating magnification of the cue’s incentive salience. Only cue-triggered ‘wanting’ was enhanced by this dopamine-related stimulation. By contrast, ‘liking’ reactions to sucrose were not amplified by amphetamine microinjections in NAc (not shown). Drug-induced sensitization of NAc-related systems produces a similar pattern of effects that lasts much longer. Modified from [47].

Figure 5

Incentive-sensitization model of addiction. Schematic model of how ‘wanting’ to take drugs may grow over time independently of ‘liking’ for drug pleasure as an individual becomes an addict. The transition from casual drug use to compulsive addiction is posited to be owing to drug-induced sensitization of mesocorticolimbic mechanisms of incentive salience. Modified from [42].

Figure 6

Separation of CS incentive value (wanting) from CS predictive value (learning) by mesolimbic activation (induced by sensitization or acute amphetamine administration). This profile analysis of neuronal firing patterns in ventral pallidum shows shifts toward CS incentive coding by either form of mesolimbic activation, and additive interaction when sensitization and amphetamine after were combined. Ordinarily neurons maximally signal predictive value (firing maximally to CS + 1 of a series of three stimuli: CS + 1 sound, CS + 2 sound, UCS sugar). Sensitization and amphetamine administration each shift neuronal coding preference toward incentive signaling (firing maximally to the CS + 2), and away from predictive signaling (without altering signals for the hedonic impact of the sugar UCS). Modified from [61•].