Dominant role of mitochondria in protection against a delayed neuronal Ca2+ overload induced by endogenous excitatory amino acids following a glutamate pulse

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 cell...

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Veröffentlicht in:FEBS letters 1996-09, Vol.393 (1), p.135-138
Hauptverfasser: Khodorov, B., Pinelis, V., Storozhevykh, T., Vergun, O., Vinskaya, N.
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container_start_page 135
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creator Khodorov, B.
Pinelis, V.
Storozhevykh, T.
Vergun, O.
Vinskaya, N.
description 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.
doi_str_mv 10.1016/0014-5793(96)00873-3
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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. 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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.</description><subject>[Ca2+]i</subject><subject>[Na+]i, the cytosolic Ca2</subject><subject>Animals</subject><subject>ANT, antimycin A</subject><subject>Antimycin A - metabolism</subject><subject>AP-5, 2-amino-5-phosphonopentanoic acid</subject><subject>Ca2+ overload</subject><subject>Calcium - metabolism</subject><subject>Cells, Cultured</subject><subject>Cerebellum - cytology</subject><subject>Cerebellum - drug effects</subject><subject>Cultured neuron</subject><subject>DCE, delayed [Ca2+]i elevation</subject><subject>EAA, excitatory amino acids</subject><subject>Endogenous excitatory amino acid</subject><subject>Excitatory Amino Acids - pharmacology</subject><subject>FCCP, carbonyl cyanide p-trifluoromethoxyphenylhydrazone</subject><subject>Fura-2/AM, acetoxymethyl ester of fura-2</subject><subject>GLU, glutamate</subject><subject>Glutamates - pharmacology</subject><subject>HBSS, HEPES-buffered salt solution</subject><subject>HEPES, 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondrial Ca2+ uptake</subject><subject>Na+ concentrations, respectively</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>NMDA, N-methy-d-aspartate</subject><subject>NMDG, N-methy-d-glucamine</subject><subject>OLIG, oligomycin</subject><subject>Oligomycins - metabolism</subject><subject>Potassium - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><issn>0014-5793</issn><issn>1873-3468</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kclO3EAQhlsoiAzLGxCpjkHRhF48Xo5hwkAkJC7hbJXdZdNRu9uy24AfhndNm0FzquWrRfUXY5eC_xRcpNeci2S9yQr1vUivOM8ztVZHbCU-nCTNv7DVoeQrOx3HfzzGuShO2Eme8yRJ5Iq9__adcegCDN4S-AY6E3z97J0eDIJx0A8-UB2Md4AtGjcGQNBkcSYNjqbBO7SwRfkD_AsN1qOObXqqI65mIKd9S85PI9BbbQIGP8yAcakHrI0eofHW-lfj2ji3tVPADgNBP9mRztlxg9FefNoz9rS7_bu9Xz883v3Z_npY9zKJ18pCIlU1iVSTjodRrqo8JYqOxEYSZo1Qhc5QNJusEptMpDViIopNqrmWpM7Yt_3cfqo60mU_mA6HufyUKfLdnr8aS_MBC14unygXmctF5rJYgviAUpW72xu5gCVfpB9Zpf4DLtGCIQ</recordid><startdate>19960909</startdate><enddate>19960909</enddate><creator>Khodorov, B.</creator><creator>Pinelis, V.</creator><creator>Storozhevykh, T.</creator><creator>Vergun, O.</creator><creator>Vinskaya, N.</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>19960909</creationdate><title>Dominant role of mitochondria in protection against a delayed neuronal Ca2+ overload induced by endogenous excitatory amino acids following a glutamate pulse</title><author>Khodorov, B. ; Pinelis, V. ; Storozhevykh, T. ; Vergun, O. ; Vinskaya, N.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p2473-292aebce16ded044e83b86ee4e82af2ea7f139d7a1f57b15716caa41956d0d2e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>[Ca2+]i</topic><topic>[Na+]i, the cytosolic Ca2</topic><topic>Animals</topic><topic>ANT, antimycin A</topic><topic>Antimycin A - metabolism</topic><topic>AP-5, 2-amino-5-phosphonopentanoic acid</topic><topic>Ca2+ overload</topic><topic>Calcium - metabolism</topic><topic>Cells, Cultured</topic><topic>Cerebellum - cytology</topic><topic>Cerebellum - drug effects</topic><topic>Cultured neuron</topic><topic>DCE, delayed [Ca2+]i elevation</topic><topic>EAA, excitatory amino acids</topic><topic>Endogenous excitatory amino acid</topic><topic>Excitatory Amino Acids - pharmacology</topic><topic>FCCP, carbonyl cyanide p-trifluoromethoxyphenylhydrazone</topic><topic>Fura-2/AM, acetoxymethyl ester of fura-2</topic><topic>GLU, glutamate</topic><topic>Glutamates - pharmacology</topic><topic>HBSS, HEPES-buffered salt solution</topic><topic>HEPES, 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondrial Ca2+ uptake</topic><topic>Na+ concentrations, respectively</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>NMDA, N-methy-d-aspartate</topic><topic>NMDG, N-methy-d-glucamine</topic><topic>OLIG, oligomycin</topic><topic>Oligomycins - metabolism</topic><topic>Potassium - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Khodorov, B.</creatorcontrib><creatorcontrib>Pinelis, V.</creatorcontrib><creatorcontrib>Storozhevykh, T.</creatorcontrib><creatorcontrib>Vergun, O.</creatorcontrib><creatorcontrib>Vinskaya, N.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>FEBS letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Khodorov, B.</au><au>Pinelis, V.</au><au>Storozhevykh, T.</au><au>Vergun, O.</au><au>Vinskaya, N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dominant role of mitochondria in protection against a delayed neuronal Ca2+ overload induced by endogenous excitatory amino acids following a glutamate pulse</atitle><jtitle>FEBS letters</jtitle><addtitle>FEBS Lett</addtitle><date>1996-09-09</date><risdate>1996</risdate><volume>393</volume><issue>1</issue><spage>135</spage><epage>138</epage><pages>135-138</pages><issn>0014-5793</issn><eissn>1873-3468</eissn><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.</abstract><cop>England</cop><pmid>8804442</pmid><doi>10.1016/0014-5793(96)00873-3</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record>
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subjects [Ca2+]i
[Na+]i, the cytosolic Ca2
Animals
ANT, antimycin A
Antimycin A - metabolism
AP-5, 2-amino-5-phosphonopentanoic acid
Ca2+ overload
Calcium - metabolism
Cells, Cultured
Cerebellum - cytology
Cerebellum - drug effects
Cultured neuron
DCE, delayed [Ca2+]i elevation
EAA, excitatory amino acids
Endogenous excitatory amino acid
Excitatory Amino Acids - pharmacology
FCCP, carbonyl cyanide p-trifluoromethoxyphenylhydrazone
Fura-2/AM, acetoxymethyl ester of fura-2
GLU, glutamate
Glutamates - pharmacology
HBSS, HEPES-buffered salt solution
HEPES, 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid
Mitochondria - drug effects
Mitochondria - metabolism
Mitochondrial Ca2+ uptake
Na+ concentrations, respectively
Neurons - drug effects
Neurons - metabolism
NMDA, N-methy-d-aspartate
NMDG, N-methy-d-glucamine
OLIG, oligomycin
Oligomycins - metabolism
Potassium - pharmacology
Rats
Rats, Wistar
title Dominant role of mitochondria in protection against a delayed neuronal Ca2+ overload induced by endogenous excitatory amino acids following a glutamate pulse
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