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Selective Modulation of Voltage-Gated Calcium Channels in the Terminal Nerve Gonadotropin-Releasing Hormone Neurons of a Teleost, the Dwarf Gourami (Colisa lalia)

Laboratory of Biological Signaling, Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan

Address all correspondence and requests for reprints to: Dr. Yoshitaka Oka, Department of Biological Sciences, Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. E-mail: okay{at}biol.s.u-tokyo.ac.jp.

GnRH neurons in the terminal nerve (TN) have been suggested to function as a neuromodulatory system that regulates long-lasting changes in the animal behavior. Here we examined electrophysiological properties of TN-GnRH neurons in a teleost (dwarf gourami, Colisa lalia), focusing on the voltage-gated Ca²⁺ channels, which are thought to be coupled to several cellular events such as GnRH release. TN-GnRH neurons showed low-voltage activated (LVA) currents and three types of pharmacologically distinct high-voltage activated (HVA) currents. The L- and N-type currents constituted 30.7 ± 3.1 and 41.0 ± 3.9%, respectively, of HVA currents, which was recorded at the holding potential of –60 mV to inactivate the LVA currents. Although P/Q-type current was small and negligible, R-type current accounted for the remaining 23.6 ± 1.6% of HVA currents. Next we examined the possibility of Ca²⁺ channel modulation induced by GnRH released in a paracrine/autocrine manner. HVA currents of up to 40% was inhibited by the application of salmon GnRH, which is the same molecular species of GnRH as is synthesized by TN-GnRH neurons themselves. However, salmon GnRH had no measurable effects on LVA currents. The inhibition of HVA currents had a dose dependence (EC₅₀ was 11.5 nM) and type specificity among different HVA currents; N- and R-type currents were preferentially inhibited, but L-type currents had by far lower sensitivity. The physiological significance of different Ca²⁺ influx pathways, and their paracrine/autocrine regulation mechanisms in TN-GnRH neurons are discussed.

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