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This version published online on November 14, 2003
Endocrinology, doi:10.1210/en.2003-1333
A more recent version of this article appeared on February 1, 2004
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Submitted on October 6, 2003
Accepted on November 4, 2003

Endogenous GABA release inhibits the firing of adult GnRH neurons

Seong-Kyu Han1, Martin G Todman1, and Allan E. Herbison1*

1 Laboratory of Neuroendocrinology, The Babraham Institute, Cambridge, CB2 4AT, UK and; Centre for Neuroendocrinology and Department of Physiology, University of Otago School of Medical Sciences, P.O. Box 913, Dunedin, New Zealand.

* To whom correspondence should be addressed. E-mail: allan.herbison{at}stonebow.otago.ac.nz.

The effect of endogenous GABAA receptor-mediated signaling on the excitability of adult male and female gonadotropin-releasing hormone (GnRH) neurons was examined using gramicidin perforated-patch electrophysiology in GnRH-LacZ and GnRH-GFP 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 2 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.
Key words: GABA • GFP • GnRH • LHRH • transgenic • patch-clamp




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