Synaptic glutamate release by ventromedial hypothalamic neurons is part of the neurocircuitry that prevents hypoglycemia.

Abstract:

:The importance of neuropeptides in the hypothalamus has been experimentally established. Due to difficulties in assessing function in vivo, the roles of the fast-acting neurotransmitters glutamate and GABA are largely unknown. Synaptic vesicular transporters (VGLUTs for glutamate and VGAT for GABA) are required for vesicular uptake and, consequently, synaptic release of neurotransmitters. Ventromedial hypothalamic (VMH) neurons are predominantly glutamatergic and express VGLUT2. To evaluate the role of glutamate release from VMH neurons, we generated mice lacking VGLUT2 selectively in SF1 neurons (a major subset of VMH neurons). These mice have hypoglycemia during fasting secondary to impaired fasting-induced increases in the glucose-raising pancreatic hormone glucagon and impaired induction in liver of mRNAs encoding PGC-1alpha and the gluconeogenic enzymes PEPCK and G6Pase. Similarly, these mice have defective counterregulatory responses to insulin-induced hypoglycemia and 2-deoxyglucose (an antimetabolite). Thus, glutamate release from VMH neurons is an important component of the neurocircuitry that functions to prevent hypoglycemia.

journal_name

Cell Metab

journal_title

Cell metabolism

authors

Tong Q,Ye C,McCrimmon RJ,Dhillon H,Choi B,Kramer MD,Yu J,Yang Z,Christiansen LM,Lee CE,Choi CS,Zigman JM,Shulman GI,Sherwin RS,Elmquist JK,Lowell BB

doi

10.1016/j.cmet.2007.04.001

subject

Has Abstract

pub_date

2007-05-01 00:00:00

pages

383-93

issue

5

eissn

1550-4131

issn

1932-7420

pii

S1550-4131(07)00096-4

journal_volume

5

pub_type

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