Gq-mER signaling has opposite effects on hypothalamic orexigenic and anorexigenic neurons

•17β-Estradiol (E2) rapidly alters the membrane excitability of hypothalamic neurons.•E2 decreases GABAergic inhibition of POMC neurons via Gq-mER.•E2 increases GABAergic inhibition of NPY/AgRP neurons via Gq-mER.•E2 decreases GABAergic inhibition of NPY/AgRP neurons via ERα.•Gq-mER also plays a role in thermoregulation in mammals.

Two populations of cells within the hypothalamus exert opposite actions on food intake: proopiomelanocortin (POMC) neurons decrease it, while neuropeptide Y (NPY)/agouti-related peptide (AgRP) neurons increase it. 17β-Estradiol (E2) is a potent anorexigenic hormone that exerts both genomic and non-genomic, rapid actions on these metabolic neurons. This review focuses on the rapid membrane effects of E2 in both POMC and NPY/AgRP neurons and how these combined effects mediate the anorexigenic effects of this steroid.