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. Author manuscript; available in PMC: 2012 Dec 10.
Published in final edited form as: J Neuroendocrinol. 2011 Jul;23(7):557–569. doi: 10.1111/j.1365-2826.2011.02145.x

Figure 1.

Figure 1

Schematic representation of GABA signaling at the GnRH neuron in the mouse. GABA terminals (grey) synapsing on GnRH neurons (green) are likely to have GABAB receptors that act to inhibit calcium entry to the terminal, thereby suppressing presynaptic activity. GABA released from the nerve terminal activates postsynaptic GABAA receptors within the synapse to generate a fast phasic depolarising or hyperpolarising response and also GABAB receptors that activate potassium channels that hyperpolarise the membrane. Spill-over of GABA from the synapse activates extrasynaptic GABAA receptors (expressing the delta receptor subunit) that provide a low level tonic influence on membrane polarisation.