Abstract
The objective of this study was to evaluate the contribution of mitochondria to the clearance of Ca2+ loads induced by glutamate or 25 mM K+ pulses. The mitochondrial Ca2+ uptake was suppressed by application of 0.5 μM antimycin A or 3–5 mM NaCN in combination with 2.5 μg/ml oligomycin. In most cells such treatments both in the presence and in the absence of external Na+ failed to abolish the early fast phase of [Ca2+] i recovery following a 1‐min 100 μM glutamate pulse. However, the late slow phase of [Ca2+] i recovery in the presence of mitochondrial poisons was transformed into a delayed [Ca2+] i elevation culminating in the neuronal Ca2+ overload. Suppression of the Na+/Ca2+ exchange caused by glutamate‐induced [Na+] i elevation promoted the development of delayed Ca2+ increase. Under identical conditions, the high [Ca2+] i transient induced by 25 mM K+ was never accompanied by a delayed Ca2+ elevation. The glutamate‐induced delayed Ca2+ increase could be readily abolished by the removal of external Ca2+ or by application in the post‐glutamate period of the antagonist of NMDA receptors, 100–200 μM AP‐5. The results obtained suggest that mitochondria play a dominant role in the protection against the neuronal Ca2+ overload induced by endogenous excitatory amino acids released in response to a short‐term glutamate challenge.
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Dates
Type | When |
---|---|
Created | 22 years, 4 months ago (April 30, 2003, 6:24 p.m.) |
Deposited | 1 year, 11 months ago (Sept. 17, 2023, 3:04 a.m.) |
Indexed | 1 month, 3 weeks ago (July 7, 2025, 1:24 a.m.) |
Issued | 28 years, 11 months ago (Sept. 9, 1996) |
Published | 28 years, 11 months ago (Sept. 9, 1996) |
Published Online | 26 years, 5 months ago (March 23, 1999) |
Published Print | 28 years, 11 months ago (Sept. 9, 1996) |
@article{Khodorov_1996, title={Dominant role of mitochondria in protection against a delayed neuronal Ca2+ overload induced by endogenous excitatory amino acids following a glutamate pulse}, volume={393}, ISSN={1873-3468}, url={http://dx.doi.org/10.1016/0014-5793(96)00873-3}, DOI={10.1016/0014-5793(96)00873-3}, number={1}, journal={FEBS Letters}, publisher={Wiley}, author={Khodorov, B. and Pinelis, V. and Storozhevykh, T. and Vergun, O. and Vinskaya, N.}, year={1996}, month=sep, pages={135–138} }