The gonadotropin-releasing hormone (GnRH) agonist-induced initial rise of bioactive LH and testosterone can be blunted in a dose-dependent manner by GnRH antagonist in the non-human primate

1992 ◽  
Vol 20 (5) ◽  
pp. 317-321 ◽  
Author(s):  
O. P. Sharma ◽  
G. F. Weinbauer ◽  
H. M. Behre ◽  
E. Nieschlag
Keyword(s):  
Gnrh Agonist ◽  
Gnrh Antagonist ◽  
Gonadotropin Releasing Hormone ◽  
Dependent Manner ◽  
Releasing Hormone ◽  
Initial Rise ◽  
Dose Dependent ◽  
Human Primate

Modulation of Pacemaker Activity by Salmon Gonadotropin-Releasing Hormone (sGnRH) in Terminal Nerve (TN)-GnRH Neurons

2000 ◽  
Vol 83 (5) ◽  
pp. 3196-3200 ◽  
Author(s):  
Hideki Abe ◽  
Yoshitaka Oka
Keyword(s):  
Late Phase ◽  
Gonadotropin Releasing Hormone ◽  
Pacemaker Activity ◽  
Dependent Manner ◽  
Releasing Hormone ◽  
Terminal Nerve ◽  
Bath Application ◽  
Gnrh Neurons ◽  
G Protein Coupled ◽  
Dose Dependent

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-β-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).

Electrophysiological Analysis of the Inhibitory Effects of FMRFamide-Like Peptides on the Pacemaker Activity of Gonadotropin-Releasing Hormone Neurons

2010 ◽  
Vol 104 (6) ◽  
pp. 3518-3529 ◽  
Author(s):  
Takeshi H. Saito ◽  
Ryo Nakane ◽  
Yasuhisa Akazome ◽  
Hideki Abe ◽  
Yoshitaka Oka
Keyword(s):  
Reversal Potential ◽  
Membrane Conductance ◽  
Gonadotropin Releasing Hormone ◽  
Pacemaker Activity ◽  
Dependent Manner ◽  
Releasing Hormone ◽  
Bath Application ◽  
Gnrh Neurons ◽  
G Protein Coupled ◽  
Dose Dependent

Gonadotropin-releasing hormone (GnRH) neurons in the terminal nerve (TN) show endogenous pacemaker activity, which is suggested to be dependent on the physiological conditions of the animal. The TN-GnRH neurons have been suggested to function as a neuromodulatory neuron that regulates long-lasting changes in the animal behavior. It has been reported that the TN-GnRH neurons are immunoreactive to FMRFamide. Here, we find that the pacemaker activity of TN-GnRH neuron is inhibited by FMRFamide: bath application of FMRFamide decreased the frequency of pacemaker activity of TN-GnRH neurons in a dose-dependent manner. This decrease was suppressed by a blockage of G protein–coupled receptor pathway by GDP-β-S. In addition, FMRFamide induced an increase in the membrane conductance, and the reversal potential for the FMRFamide-induced current changed according to the changes in [K+]out as predicted from the Nernst equation for K+. We performed cloning and sequence analysis of the PQRFamide (NPFF/NPAF) gene in the dwarf gourami and found evidence to suggest that FMRFamide-like peptide in TN-GnRH neurons of the dwarf gourami is NPFF. NPFF actually inhibited the pacemaker activity of TN-GnRH neurons, and this inhibition was blocked by RF9, a potent and selective antagonist for mammalian NPFF receptors. These results suggest that the activation of K+ conductance by FMRFamide-like peptide (≈NPFF) released from TN-GnRH neurons themselves causes the hyperpolarization and then inhibition of pacemaker activity in TN-GnRH neurons. Because TN-GnRH neurons make tight cell clusters in the brain, it is possible that FMRFamide-like peptides released from TN-GnRH neurons negatively regulates the activities of their own (autocrine) and/or neighboring neurons (paracrine).

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