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Laboratory of Neuroendocrinology (S.-K.H., M.G.T., A.E.H.), The Babraham Institute, Cambridge CB2 4AT, United Kingdom; and Centre for Neuroendocrinology and Department of Physiology (S.-K.H., A.E.H.), University of Otago School of Medical Sciences, Dunedin, New Zealand
Address all correspondence and requests for reprints to: Allan E. Herbison, Department of Physiology, University of Otago School of Medical Sciences, P.O. Box 913, Dunedin, New Zealand. E-mail: allan.herbison{at}stonebow.otago.ac.nz.
Abstract
The effect of endogenous 
-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 GABAA receptor antagonist bicuculline (20 µM) 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 GABAA receptor exerts a powerful net inhibitory effect upon the excitability of mature GnRH neurons.
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