Activation of gonadotropin-releasing hormone receptors produces neuronal excitation in the rat hippocampus

Whole-cell patch-clamp recordings of evoked action potentials were made in CA1 and CA3 pyramidal neurons of rat hippocampal slices. Previously we have demonstrated that activation of gonadotropin-releasing hormone (GnRH) receptors induces a long-lasting enhancement of synaptic transmission mediated by ionotropic glutamate receptors in CA1 pyramidal neurons of rat hippocampal slices. Here, we further studied whether activation of GnRH receptors could modulate intrinsic neuronal excitability in CA1 and CA3 pyramidal neurons of rat hippocampal slices. The use of a specific GnRH analog, leuprolide (10 ^-8 M), elicited a relatively long-term increase in evoked action potentials in CA1 and CA3 pyramidal neurons, respectively. The GnRH receptor-induced increase in evoked action potentials in both CA1 and CA3 pyramidal neurons could be abolished by a potent GnRH receptor antagonist, [acetyl-3,4-dehydro-Pro ¹ ,D-p-F-Phe ² ,D-Trp ^3,6 ]-LHRH (10 ^-8 M). The present study suggests that activation of GnRH receptors can lead to an increase of intrinsic neuronal excitability of both CA1 and CA3 pyramidal neurons in the rat hippocampus, an important integrative region for reproductive process, both endocrinologically and behaviorally.