DOI: 10.1101/517797Jan 11, 2019Paper

Insulin enhances presynaptic glutamate release in the nucleus accumbens via opioid receptor-mediated disinhibition

BioRxiv : the Preprint Server for Biology
Max F OginskyCarrie R Ferrario

Abstract

Insulin influences learning and cognition and activity in brain centers that mediate reward and motivation in humans. However, very little is known about how insulin influences excitatory transmission within brain reward centers such as the nucleus accumbens (NAc). Further, insulin dysregulation that accompanies obesity is linked to cognitive decline, depression, anxiety, and aberrant motivation that also rely on excitatory transmission in the NAc, but potential mechanisms are poorly understood. Here we show that insulin receptor activation increases presynaptic glutamate release via a previously unidentified form of opioid receptor-mediated disinhibition, whereas activation of IGF receptors by insulin decreases presynaptic glutamate release in the NAc. Furthermore, obesity results in a loss of the insulin receptor-mediated increases and a reduction in NAc insulin receptor surface expression, while preserving reductions in excitatory transmission mediated by IGF receptors. These results provide the first insights into how insulin influences excitatory transmission in the adult brain and have broad implications for the regulation of motivation and reward related processes by peripheral hormones.

Related Concepts

Brain
Cognition
Mental Depression
Hormones
Insulin
Learning
Motivation
Nucleus Accumbens
Obesity
Opioid Receptor

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