Insulin excites anorexigenic proopiomelanocortin neurons via activation of canonical transient receptor potential channels.

ABSTRACT: Proopiomelanocortin (POMC) neurons within the hypothalamic arcuate nucleus are vital anorexigenic neurons. Although both the leptin and insulin receptors are coupled to the activation of phosphatidylinositide 3 kinase (PI3K) in POMC neurons, they are thought to have disparate actions on POMC excitability. Using whole-cell recording and selective pharmacological tools, we have found that, similar to leptin, purified insulin depolarized POMC and adjacent kisspeptin neurons via activation of TRPC5 channels, which are highly expressed in these neurons. In contrast, insulin hyperpolarized and inhibited NPY/AgRP neurons via activation of KATP channels. Moreover, Zn(2+), which is found in insulin formulations at nanomolar concentrations, inhibited POMC neurons via activation of KATP channels. Fin

SUBMITTER: Qiu J 

PROVIDER: S-EPMC4183666 | biostudies-literature | 2014 Apr

REPOSITORIES: biostudies-literature