| Abstract | Gonadotropin-releasing hormone (GnRH) neurons secrete in a circhoral pulsatile pattern required for normal reproductive function. Their electrophysiology and second messenger signaling has been extensively studied. A plausible mechanism for GnRH pulsatility has been proposed, involving autoregulation of GnRH neurons through GnRH receptors (hereafter referred to as the autocrine mechanism). Mathematical models have been developed to explain certain features of each of these, separately. The slow nature of the GnRH rhythm suggests that many faster processes in these neurons could be involved. In particular, the role of electrical activity and calcium dynamics in rhythmogenesis is not clear. The goals of the present work are twofold. First, we examine two mechanisms for phasic electrical activity in GnRH neurons. Second, we present some preliminary findings from coupling the electrophysiological model to an existing model for GnRH pulsatility. |
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