The peptidergic neurons play important roles such as neuromodulatory and neuroendocrine functions in the central nervous system. However, our knowledge about the organization and the function of the peptidergic neuromodulator systems is still very poor. The terminal nerve GnRH peptidergic neurons of a teleost, the dwarf gourami (Colisa lalia), serve as an excellent model system for such study. The cell bodies are large and make up a tight cell cluster, and the easy access to the cell bodies on the ventral surface of the brain makes the electrophysiological measurements in a precisely controlled manner. Here we show direct evidence to demonstrate the electrical coupling and the synchronization of the neural firing activity among the terminal nerve GnRH neurons by using the double patch-clamp recording technique. The electrical coupling coefficient was strong enough (ranged from 0.083 to 0.370) to synchronize spontaneous firings of GnRH neurons in the cluster. A model, in which the firings in the cluster occur within a small time window (dozens of milliseconds), was verified by using the serial loose-seal extracellular patch-clamp recordings and the cross-correlogram analysis. The present findings provide several insights for understanding the physiological mechanisms and functional significance of synchronized activities in the peptidergic and/or aminergic neuromodulator system as well as in the peptidergic neuroendocrine cells.

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.