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Characterization of the hypo‐osmolarity‐induced Ca 2+ response in cultured rat astrocytes
Author(s) -
Fischer Richard,
Schliess Freimut,
Häussinger Dieter
Publication year - 1997
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/(sici)1098-1136(199705)20:1<51::aid-glia5>3.0.co;2-8
Subject(s) - osmotic concentration , thapsigargin , bapta , biology , phospholipase c , calcium , endocrinology , medicine , ryanodine receptor , cytosol , phospholipase , biophysics , biochemistry , intracellular , signal transduction , enzyme
The influence of astrocyte swelling on the cytosolic free calcium concentration [Ca 2+ ] i was studied at the single cell level. Sudden exposure of normo‐osmotically (305 mosmol/l) cultured astrocytes to hypo‐osmotic medium induced a biphasic increase in cytosolic calcium with an initial peak followed by a sustained plateau. The response was osmolarity dependent and was maximal at 205 mosmol/l with respect to [Ca 2+ ] i and the percentage of responding cells. Other modes of astrocyte swelling [gradual adjustment of hypo‐osmolarity, normo‐osmotic exposure of hyper‐osmotic (405 mosmol/l) maintained cells] produced a much weaker [Ca 2+ ] i response. Change from 405 to 205 mosmol/l, however, resulted in the entire peak and an increased plateau. Experiments with Ca 2+ ‐free medium and after pretreatment with BAPTA‐AM, thapsigargin, phorbol myristate acetate, or nimodipine revealed that the peak mainly resulted from depletion of intracellular Ca 2+ stores, whereas the plateau was probably due to capacitative Ca 2+ entry and Ca 2+ influx independent of store depletion including a nimodipin‐sensitive component. Prior depletion of ryanodine‐, bradykinin‐ or ATP‐sensitive stores revealed that the initial hypo‐osmolarity‐induced Ca 2+ ‐release was from a Ca 2+ pool also affected by ATP and bradykinin, but not by ryanodine. The recent finding, that the hypo‐osmolarity‐induced [Ca 2+ ] i response was completely maintained if phospholipase C‐mediated phosphatidylinositol hydrolysis was blocked, suggests that hypo‐osmolarity may exert an inositol (1,4,5) triphosphate‐independent access to these stores. GLIA 20:51‐58, 1997. © 1997 Wiley‐Liss, Inc.