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The Journal of Neurophysiology Vol. 83 No. 5 May 2000, pp. 3196-3200
Copyright ©2000 by the American Physiological Society
RAPID COMMUNICATION
Misaki Marine Biological Station, Graduate School of Science, University of Tokyo, Kanagawa 238-0225, Japan
Abe, Hideki and
Yoshitaka Oka.
Modulation of Pacemaker Activity by Salmon Gonadotropin-Releasing
Hormone (sGnRH) in Terminal Nerve (TN)-GnRH Neurons. J. Neurophysiol. 83: 3196-3200, 2000. The
terminal nerve (TN)-gonadotropin-releasing hormone (GnRH) neurons
project widely in the brain instead of the pituitary and show
endogenous pacemaker activity that is dependent on the physiological
conditions of the animal. We suggest that the TN-GnRH system may act as
a putative neuromodulator that is involved in the regulation of many
long-lasting changes in the animal's behavior. In the present study,
we find that the pacemaker activity of TN-GnRH neurons is modulated by
salmon GnRH (sGnRH), which is the same molecular species of GnRH
peptide produced by TN-GnRH neurons themselves. Bath application of
sGnRH (2-200 nM) transiently decreased (early phase) and then
subsequently increased (late phase) the frequency of pacemaker activity
of TN-GnRH neurons in a dose-dependent manner. These biphasic changes
of pacemaker activities were suppressed by intracellular application of
guanosin 5'-0-(2-thiodi-phosphate) (GDP-
-S). The results
suggest that G-protein coupled receptors are present on the cell
surface and play a triggering role in modulating the frequency of
pacemaker activities in TN-GnRH neurons. Because the TN-GnRH neurons
make tight cell clusters with no intervening glial cells, it may be
further suggested that GnRH released from GnRH neurons regulates the
activities of their own (autocrine) and/or neighboring GnRH neurons (paracrine).
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