INCREASE OF INTRACELLULAR CALCIUM-INDUCED BY OXYTOCIN IN HYPOTHALAMIC CULTURED ASTROCYTES

被引:31
作者
DISCALAGUENOT, D
MOUGINOT, D
STROSSER, MT
机构
[1] Institut de Physiologie (URA 1446 CNRS), Université Louis Pasteur, Strasbourg
关键词
CULTURE; HYPOTHALAMUS; MICROSPECTROFLUOROMETRY;
D O I
10.1002/glia.440110308
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
A recent study demonstrated oxytocin (OT) receptors on hypothalamic cultured astrocytes (Di Scala-Guenot and Strosser, 1992). The attempt in the present paper was to determine a possible intracellular calcium mobilization induced by OT receptor activation in these cells. Using the microspectrofluorimetric technique with fura-2 as calcium indicator, brief applications of OT on single astrocytes induced a transient and reversible dose-dependent increase of intracellular calcium concentration ([CA(2+)](i)) in most of the cells tested. In a few cells, OT application triggered intracellular calcium oscillations. Repetitive applications of OT generally produced a decreasing calcium signal, suggesting a desensitization of the receptor. OT-induced calcium release was prevented by a prior or simultaneous application of an OT antagonist. The origin of the calcium mobilization was assessed during conditions where no extracellular calcium was available. Neither removal of extracellular calcium nor addition of a calcium channel blocker, cadmium 100 mu M, in the bathing solution, did affect the calcium response to OT, demonstrating that release of intracellular calcium is solely involved in the OT-induced [Ca2+](i) increase. The OT-induced calcium mobilization was abolished after thapsigargin application (100 nM). This indicates that the calcium response to OT application was principally associated with activation of the IP3-sensitive calcium stores. Taken together these results demonstrate that OT receptors previously detected on hypothalamic cultured astrocytes are functional receptors which transduction pathways involve calcium mobilization from IP3-sensitive stores. (C) 1994 Wiley-Liss, Inc.
引用
收藏
页码:269 / 276
页数:8
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