Dantrolene Prevents Glutamate Cytotoxicity and Ca 2+ Release from Intracellular Stores in Cultured Cerebral Cortical Neurons

Dantrolene Prevents Glutamate Cytotoxicity and Ca 2+ Release from Intracellular Stores in... Abstract: Using primary cultures of cerebral cortical neurons, it has been demonstrated that the antihyperthermia drug dantrolene completely protects against glutamate‐induced neurotoxicity. Furthermore, in the presence of extracellular calcium, dantrolene reduced the glutamate‐induced increase in the intracellular calcium concentration by 70%. In the absence of extracellular calcium, this glutamate response was completely blocked by dantrolene. Dantrolene did not affect the kinetics of (3H)glutamate binding to membranes prepared from similar cultures. These results indicate that release of calcium from intracellular stores is essential for the propagation of glutamate‐induced neuronal damage. Because it is likely that glutamate is involved in neuronal degeneration associated with ischemia and hypoxia, the present findings might suggest that dantrolene and possibly other drugs affecting intracellular calcium pools might be of therapeutic interest. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neurochemistry Wiley

Dantrolene Prevents Glutamate Cytotoxicity and Ca 2+ Release from Intracellular Stores in Cultured Cerebral Cortical Neurons

Journal of Neurochemistry, Volume 56 (3) – Mar 1, 1991

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Publisher
Wiley
Copyright
Copyright © 1991 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0022-3042
eISSN
1471-4159
DOI
10.1111/j.1471-4159.1991.tb02031.x
Publisher site
See Article on Publisher Site

Abstract

Abstract: Using primary cultures of cerebral cortical neurons, it has been demonstrated that the antihyperthermia drug dantrolene completely protects against glutamate‐induced neurotoxicity. Furthermore, in the presence of extracellular calcium, dantrolene reduced the glutamate‐induced increase in the intracellular calcium concentration by 70%. In the absence of extracellular calcium, this glutamate response was completely blocked by dantrolene. Dantrolene did not affect the kinetics of (3H)glutamate binding to membranes prepared from similar cultures. These results indicate that release of calcium from intracellular stores is essential for the propagation of glutamate‐induced neuronal damage. Because it is likely that glutamate is involved in neuronal degeneration associated with ischemia and hypoxia, the present findings might suggest that dantrolene and possibly other drugs affecting intracellular calcium pools might be of therapeutic interest.

Journal

Journal of NeurochemistryWiley

Published: Mar 1, 1991

References

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