| Autor: |
Prevarskaya, N., Skryma, R., Vacher, P., Bresson-Bepoldin, L., Odessa, M.F., Rivel, J., San Galli, F., Guerin, J., Dufy-Barbe, L. |
| Zdroj: |
Molecular and Cellular Neurosciences; December 1994, Vol. 5 Issue: 6 p699-708, 10p |
| Abstrakt: |
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+]iwas 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+]idue to Ca2+entry through plasma membrane voltage-sensitive L-type Ca2+channels. Protein kinase C (PKC) depletion induced by a pretreatment with 1 μMPMA for 24 h abolished spontaneous Ca2+transients and the action of GnRH on [Ca2+]iand Ca2+channels. Phloretin (250 μMand 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+]iin stimulated and unstimulated NS adenoma cells. |
| Databáze: |
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