Licking microstructure in response to novel rewards, reward devaluation and dopamine antagonists: Possible role of D1 and D2 medium spiny neurons in the nucleus accumbens

Evidence on the effect of dopamine D1 and D2-like antagonists and of manipulations of reward value on licking microstructure is reanalysed considering recent findings on the role of nucleus accumbens (NAc) medium spiny neurons (MSNs) in the control of sugar intake. The results of this analysis suggest that D1 MSN activation, which is involved in the emission of licking bursts, might play a crucial role in response to novel rewards. D2 MSN activation, which results in reduction of burst size and suppression of licking, might mediate the response to reward devaluation. Elucidating the neural mechanisms underlying the licking response might lead to a better definition of its microstructural measures in behaviourally and psychologically meaningful functional terms. This could further support its use as a behavioural substrate in the study of the neural mechanisms of ingestive behaviour and motivation, as well as in animal models of pathological conditions such as eating disorders and obesity. • D2 antagonists induce extinction mimicry on licking burst number time-course. • D1 antagonists mimic the response to a smaller reward without reward devaluation. • Ablation of D1 and activation of D2 MSNs mimic D1 and D2 antagonists, respectively. • D1 MSN activation might increase licking burst number in response to novel rewards. • D2 MSN activation might sense reward devaluation yielding reduced licking burst size.