Adiponectin regulates
glucose and lipid metabolism, acting against
atherosclerosis and
metabolic syndrome. Accumulating evidences suggest that
adiponectin acts on the brain including the arcuate nucleus of hypothalamus (
ARC). The
ARC contains orexigenic
neuropeptide Y (NPY)/agouti related
peptide (AgRP) neurons and anorexigenic
proopiomelanocortin (
POMC) neurons, the first order neurons for feeding regulation. We recently reported that intracerebroventricular injection of
adiponectin at low
glucose level suppressed food intake, while at elevated
glucose level it promoted food intake, exhibiting
glucose-dependent reciprocal effects. As an underlying neuronal mechanism, physiological level of
adiponectin at low
glucose activated
ARC POMC neurons and at high
glucose inactivated them. Now, whether physiological level of
adiponectin also affects NPY/AgRP neurons is essential for fully understanding the
adiponectin action, but it remains to be clarified. We here report that a physiological dose of
adiponectin, in both high and low
glucose conditions, attenuated action potential firing without altering resting membrane potential in
ARC NPY neurons. This
adiponectin effect was abolished by GABAA receptor blockade.
Adiponectin enhanced amplitude but not frequency of inhibitory postsynaptic current (IPSC) onto NPY neurons. These results demonstrate that
adiponectin enhances IPSC onto NPY neurons to attenuate action potential firing in NPY neurons in a
glucose-independent manner, being contrasted to its
glucose-dependent effect on
POMC neurons.