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Article: Role of Calcium Ions in Acidosis-Induced Glial Swelling

TitleRole of Calcium Ions in Acidosis-Induced Glial Swelling
Authors
Issue Date1997
Citation
Acta Neurochirurgica, Supplement, 1997, v. 1997 n. 70, p. 144-147 How to Cite?
AbstractTissue acidosis occurring in cerebral ischemia and traumatic brain injury is a mediator of cytotoxic brain edema. In vitro, extracellular lactacidosis induces swelling of glial cells in a dose dependent manner. pH-regulatory membrane transporters and channels have been identified which are involved in the increase of the glial cell volume. Underlying mechanisms of their activation are poorly understood, however. We have, therefore, addressed the question, whether and how Ca2+-ions play a role in acidosis-induced glial swelling and intracellular acidification. For that purpose C6 glioma cells were suspended and the pH in the medium was lowered from 7.4 (baseline) to 6.2 by isotonic lactic acid. Cell volume and intracellular pH (pHi) were assessed by flow cytometry. In the presence of Ca2+-ions the cell volume reached a maximum of 125.1% from acidosis. In experiments using a calcium-free suspension medium, cell swelling from acidosis was inhibited by 74%. Additional buffering of intracellular calcium (Ca2+ i) had no further inhibitory effect on acidosis-induced cell swelling, while buffering of Ca2+ 1 by BAPTA-AM alone did not affect the glial volume increase secondary to administration of lactic acid. pH1 which was decreasing from acidosis was not affected by the experimental modifications of the Ca2+-concentration in the medium or cytosol. The present data indicate that lactacidosis-induced glial swelling depends on the presence of extracellular Ca2+-ions, while release of Ca2+-ions from intracellular stores does not seem to be involved.
Persistent Identifierhttp://hdl.handle.net/10722/149569
ISSN
2015 SCImago Journal Rankings: 0.379
References

 

DC FieldValueLanguage
dc.contributor.authorRingel, Fen_US
dc.contributor.authorPlesnila, Nen_US
dc.contributor.authorChang, RCCen_US
dc.contributor.authorPeters, Jen_US
dc.contributor.authorStaub, Fen_US
dc.contributor.authorBaethmann, Aen_US
dc.date.accessioned2012-06-26T05:55:24Z-
dc.date.available2012-06-26T05:55:24Z-
dc.date.issued1997en_US
dc.identifier.citationActa Neurochirurgica, Supplement, 1997, v. 1997 n. 70, p. 144-147en_US
dc.identifier.issn0065-1419en_US
dc.identifier.urihttp://hdl.handle.net/10722/149569-
dc.description.abstractTissue acidosis occurring in cerebral ischemia and traumatic brain injury is a mediator of cytotoxic brain edema. In vitro, extracellular lactacidosis induces swelling of glial cells in a dose dependent manner. pH-regulatory membrane transporters and channels have been identified which are involved in the increase of the glial cell volume. Underlying mechanisms of their activation are poorly understood, however. We have, therefore, addressed the question, whether and how Ca2+-ions play a role in acidosis-induced glial swelling and intracellular acidification. For that purpose C6 glioma cells were suspended and the pH in the medium was lowered from 7.4 (baseline) to 6.2 by isotonic lactic acid. Cell volume and intracellular pH (pHi) were assessed by flow cytometry. In the presence of Ca2+-ions the cell volume reached a maximum of 125.1% from acidosis. In experiments using a calcium-free suspension medium, cell swelling from acidosis was inhibited by 74%. Additional buffering of intracellular calcium (Ca2+ i) had no further inhibitory effect on acidosis-induced cell swelling, while buffering of Ca2+ 1 by BAPTA-AM alone did not affect the glial volume increase secondary to administration of lactic acid. pH1 which was decreasing from acidosis was not affected by the experimental modifications of the Ca2+-concentration in the medium or cytosol. The present data indicate that lactacidosis-induced glial swelling depends on the presence of extracellular Ca2+-ions, while release of Ca2+-ions from intracellular stores does not seem to be involved.en_US
dc.languageengen_US
dc.relation.ispartofActa Neurochirurgica, Supplementen_US
dc.subject.meshAcidosis - Physiopathologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBrain Edema - Physiopathologyen_US
dc.subject.meshBrain Injuries - Physiopathologyen_US
dc.subject.meshBrain Ischemia - Physiopathologyen_US
dc.subject.meshCalcium - Physiologyen_US
dc.subject.meshFlow Cytometryen_US
dc.subject.meshNeuroglia - Physiologyen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titleRole of Calcium Ions in Acidosis-Induced Glial Swellingen_US
dc.typeArticleen_US
dc.identifier.emailChang, RCC:rccchang@hkucc.hku.hken_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid9416304en_US
dc.identifier.scopuseid_2-s2.0-0031309172en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031309172&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume1997en_US
dc.identifier.issue70en_US
dc.identifier.spage144en_US
dc.identifier.epage147en_US
dc.publisher.placeAustriaen_US
dc.identifier.scopusauthoridRingel, F=6602136569en_US
dc.identifier.scopusauthoridPlesnila, N=7003609441en_US
dc.identifier.scopusauthoridChang, RCC=7403713410en_US
dc.identifier.scopusauthoridPeters, J=7404191248en_US
dc.identifier.scopusauthoridStaub, F=7006611117en_US
dc.identifier.scopusauthoridBaethmann, A=7004994793en_US

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