Mechanical stimulation of a single cell in a primary mixed glial cell culture induced a wave of increased intracellular calcium concentration ((Ca2+)i) that was communicated to surrounding cells. Following propagation of the Ca2+ wave, many cells showed asynchronous oscillations in (Ca2+)i. Dantrolene sodium (10 μM) inhibited the increase in (Ca2+)i associated with this Ca2+ wave by 60‐80%, and prevented subsequent Ca2+ oscillations. Despite the markedly decreased magnitude of the increase in (Ca2+)i, the rate of propagation and the extent of communication of the Ca2+ wave were similar to those prior to the addition of dantrolene. Thapsigargin (10 nM to 1 μM) induced an initial increase in (Ca2+)i ranging from 100 nM to 500 nM in all cells that was followed by a recovery of (Ca2+)i to near resting levels in most cells. Transient exposure to thapsigargin for 2 min irreversibly blocked communication of a Ca2+ wave from the stimulated cell to adjacent cells. Glutamate (50 μM) induced an initial increase in (Ca2+)i in most cells that was followed by sustained oscillations in (Ca2+)i in some cells. Dantrolene (10 μM) inhibited this initial (Ca2+)i increase caused by glutamate by 65‐90% and abolished subsequent oscillations. Thapsigargin (10 nM to 1 μm) abolished the response to glutamate in over 99% of cells. These results suggest that while both dantrolene and thapsigargin inhibit intracellular Ca2+ release, only thapsigargin affects the mechanism that mediates intercellular communication of Ca2+ waves. These findings are consistent with the hypothesis that inositol trisphosphate (IP3) mediates the propagation of Ca2+ waves whereas Ca2+ ‐induced Ca2+ release amplifies Ca2+ waves and generates subsequent Ca2+ oscillations.
Glia – Wiley
Published: Feb 1, 1993
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