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Gonadotropin-Releasing Hormone Induced Ca Influx in Nonsecreting Pituitary Adenoma Cells: Role of Voltage-Dependent Ca Channels and Protein Kinase C
Authors:NPrevarskaya  R Skryma  P Vacher  L Bresson-Bepoldin  M F Odessa  J Rivel  F San Galli  J Guerin  L Dufy-Barbe
Abstract:The action mechanism of gonadotropin-releasing hormone (GnRH) on the cytosolic free calcium concentration (Ca2+]i) and high-threshold voltage-dependent Ca2+ channel activity was studied in human nonsecreting (NS) pituitary adenoma cells. Ca2+]i was monitored in individual cells by dual emission microspectrofluorimetry using indo1 as intracellular fluorescent Ca2+ probe. The whole-cell recording patch-clamp technique was used to study Ca2+ channels. A short application of GnRH (1 to 100 nM) induced an increase in Ca2+]i due to Ca2+ entry through plasma membrane voltage-sensitive L-type Ca2+ channels. Protein kinase C (PKC) depletion induced by a pretreatment with 1 μM PMA for 24 h abolished spontaneous Ca2+ transients and the action of GnRH on Ca2+]i and Ca2+ channels. Phloretin (250 μM and staurosporine (20 nM), two protein kinase C inhibitors, inhibited Ca2+ channel activity, thereby suppressing the effect of GnRH. On the other hand, activation of PKC by a short application of phorbol myristate acetate (10 nM) stimulated Ca2+ influx through Ca2+ channels. These findings demonstrate that, in human NS adenoma cells, GnRH (1 to 100 nM) induces an increase in Ca2+]i, principally due to Ca2+ entry through L-type voltage-activated Ca2+ channels. PKC regulates this mechanism as well as basal ion channel activity, thus exerting both positive and negative control of Ca2+]i in stimulated and unstimulated NS adenoma cells.
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