Chapter VI Dopamine, motivation and reward

Abstract

Experimental manipulation of dopamine (DA) transmission by lesions and drugs indicates a role in the acquisition and expression of behavior motivated by conventional and drug reinforcers. This role is related to modulation of ionotropic transmission, mainly in the ventral striatum (n. accumbens/olfactory tubercle), in components of the so-called extended amygdala (central amygdala and bed nucleus of stria terminalis) and in the medial prefrontal cortex. DA release in the n. accumbens elicits an appetitive state (euphoria), facilitates memory consolidation in Pavlovian learning, promotes approach behavior towards novel cues and contexts and mediates the energizing action of conditioned stimuli on instrumental behavior. These functions can be related to differential stimulationof DAtransmissionbyconditionedandunconditioned motivational stimuli in different DA terminal areas. In the n. accumbens shell, DA responsiveness follows Pavlovian rules, being related to appetitive valence, novelty and unpredictability of the stimulus. In contrast, n. accumbens core and medial prefrontal cortex DA responds to both conditioned and unconditioned stimuli in relation to their generic motivational relevance. These properties conform to a role of DA in incentive arousal. This term describes the state induced by DA released in response to motivational stimuli and its widespread influence on behavior: euphoria and elevated mood, facilitation of the acquisition of incentive properties by otherwise neutral stimuli and contexts through Pavlovian associations (incentive learning), facilitation of instrumental and approach behavior by conditioned incentives. Addictive drugs share the ability to stimulate DA transmission in the ventral striatum and in particular in the accumbens shell. Various hypotheses attribute to this property a role in the mechanism of drug addiction. According to the incentive-learning hypothesis, drug addiction is the result of the excessive incentive properties acquired by drug-conditioned stimuli following maladaptive stimulation of DA transmission in the accumbens shell.