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Endocrinology. 2004 Feb;145(2):495-9. Epub 2003 Nov 14.

Endogenous GABA release inhibits the firing of adult gonadotropin-releasing hormone neurons.

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Laboratory of Neuroendocrinology, Babraham Institute, Cambridge CB2 4AT, U.K.


The effect of endogenous gamma-aminobutyric acid (GABA)(A) receptor-mediated signaling on the excitability of adult male and female GnRH neurons was examined using gramicidin perforated-patch electrophysiology in GnRH-LacZ and GnRH-GFP (green fluorescent protein) transgenic mouse models. In both lines of mice, approximately 80% of GnRH neurons (n = 42) responded to the selective GABA(A) receptor antagonist bicuculline (20 microm) with a rapid and reversible membrane depolarization and/or increase in firing rate. Approximately 16% of GnRH neurons gave no response, and two neurons were inhibited by bicuculline. The same depolarizing responses (78%) were obtained from adult gonadectomized GnRH-GFP mice. The depolarizing response to bicuculline persisted in the presence of tetrodotoxin, demonstrating that even action potential-independent GABA release was acting to reduce GnRH neuron membrane potential. These observations show that endogenous GABA signaling through the GABA(A) receptor exerts a powerful net inhibitory effect upon the excitability of mature GnRH neurons.

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