Electrophysiological recordings from gonadotrophs. Evidence for Ca2+ channels mediated by gonadotrophin-releasing hormone.
The electrophysiological properties of gonadotrophs have been studied in vitro, using the ovine adenohypophyseal pars tuberalis as a naturally enriched source of this cell type. Trypsin-dispersed pars tuberalis cells maintained in primary tissue culture had a membrane potential of -72 +/- 4 mV (mean +/- SEM) and an input resistance of 314 +/- 38 M omega. Spontaneous action potentials were not observed; however, a single spike could be induced by depolarizing current injection. The hypophysiotrophic peptide gonadotrophin-releasing hormone (GnRH) increased membrane voltage fluctuations, but these fluctuations (+/- 5-10 mV) did not induce action potentials or changes in membrane potential or resistance. Power spectra obtained from analysis of this noise indicated that the fundamental event underlying GnRH action has a mean life-time of 38.4 +/- 4.5 ms. The observations that cells incubated in recording medium secreted luteinizing hormone in response to GnRH and that the GnRH-induced increase in voltage noise was inhibited by Ca2+ channel antagonists support the hypotheses (1) that gonadotrophin secretion is initiated by GnRH-induced Ca2+ channel activation and (2) that action potentials are not a prerequisite for gonadotrophin release.
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Mason
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Waring
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002469:Cell Separation; D002478:Cells, Cultured; D004553:Electric Conductivity; D004594:Electrophysiology; D005071:Evoked Potentials / Q000187:drug effects; D066298:In Vitro Techniques; D007473:Ion Channels / Q000378:metabolism*; D007986:Luteinizing Hormone / Q000378:metabolism; D010903:Pituitary Gland, Anterior / Q000166:cytology* / Q000502:physiology; D010906:Pituitary Hormone-Releasing Hormones / Q000494:pharmacology*; D012756:Sheep
D007473:Ion Channels; D010906:Pituitary Hormone-Releasing Hormones; D007986:Luteinizing Hormone; D002118:Calcium