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Insulin enhances striatal dopamine release by activating cholinergic interneurons and thereby signals reward

Melissa A. Stouffer,Catherine A. Woods,J. Patel,Christian R. Lee,P. Witkovsky,Li Bao,R. Machold,Kymry T. Jones,Soledad Cabeza de Vaca,M. Reith,K. Carr,M. Rice

Published 2015 in Nature Communications

ABSTRACT

Insulin activates insulin receptors (InsRs) in the hypothalamus to signal satiety after a meal. However, the rising incidence of obesity, which results in chronically elevated insulin levels, implies that insulin may also act in brain centres that regulate motivation and reward. We report here that insulin can amplify action potential-dependent dopamine (DA) release in the nucleus accumbens (NAc) and caudate–putamen through an indirect mechanism that involves striatal cholinergic interneurons that express InsRs. Furthermore, two different chronic diet manipulations in rats, food restriction (FR) and an obesogenic (OB) diet, oppositely alter the sensitivity of striatal DA release to insulin, with enhanced responsiveness in FR, but loss of responsiveness in OB. Behavioural studies show that intact insulin levels in the NAc shell are necessary for acquisition of preference for the flavour of a paired glucose solution. Together, these data imply that striatal insulin signalling enhances DA release to influence food choices. Insulin signals satiety after a meal; however, the rising incidence of obesity and chronic insulin elevation suggests that insulin may also signal reward. Here, Stouffer et al. show that insulin amplifies dopamine release in rodent striatum depending on diet, and that striatal insulin can influence food choice.

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