Affective neuroscience research has revealed that reward contains separable components of 'liking', 'wanting', and learning. Here we focus on current 'liking' and 'wanting' findings and applications to clinical disorders. 'Liking' is the hedonic impact derived from a pleasant experience, and is amplified by opioid and related signals in discrete sites located in limbic-related brain areas. 'Wanting' refers to incentive salience, a motivation process for reward, and is mediated by larger systems involving mesocorticolimbic dopamine. Deficits in incentive salience may contribute to avolitional features of depression and related disorders, whereas deficits in hedonic impact may produce true anhedonia. Excesses in incentive salience, on the other hand, can lead to addiction, especially when narrowly focused on a particular target. Finally, a fearful form of motivational salience may even contribute to some paranoia symptoms of schizophrenia and related disorders.

How do brain mechanisms create maladaptive attractions? Here intense maladaptive attractions are created in laboratory rats by pairing optogenetic channelrhodopsin (ChR2) stimulation of central nucleus of amygdala (CeA) in rats with encountering either sucrose, cocaine, or a painful shock-delivering object. We find that pairings make the respective rats pursue either sucrose exclusively, or cocaine exclusively, or repeatedly self-inflict shocks. CeA-induced maladaptive attractions, even to the painful shock-rod, recruit mesocorticolimbic incentive-related circuitry. Shock-associated cues also gain positive incentive value and are pursued. Yet the motivational effects of paired CeA stimulation can be reversed to negative valence in a Pavlovian fear learning situation, where CeA ChR2 pairing increases defensive reactions. Finally, CeA ChR2 valence can be switched to neutral by pairing with innocuous stimuli. These results reveal valence plasticity and multiple modes for motivation via mesocorticolimbic circuitry under the control of CeA activation.

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