Intracellular acidification is not a prerequisite for glutamate-triggered death of cultured hippocampal neurons

Guang Jian Wang, Shauna R. Richardson, Stanley A Thayer

Research output: Contribution to journalArticlepeer-review

27 Scopus citations

Abstract

Glutamate decreased intracellular pH (pHi) in cultured rat hippocampal neurons. The protonophore, FCCP (1μM), produced an acidification comparable to that produced by glutamate. Application of glutamate to FCCP-treated cells, returned pHi to resting levels. This alkaline shift resulted from a glutamate-induced membrane depolarization that removed the driving force across the plasmalemma for H+ entry via FCCP. The endogenous protonophore, arachidonic acid (10 μM), produced pHi changes similar to those elicited by FCCP. Because application of glutamate and FCCP in combination did not change pHi, this treatment was used to determine the role of glutamate-induced acidification in neurotoxicity. FCCP (1 μM, 5 min) did not affect neuronal viability, either alone or in combination with various concentrations of glutamate, as indicated by the release of lactate dehydrogenase into the bathing medium. Thus, acidification was not the cause of glutamate-induced cell death although, it may be symptomatic of neurotoxic processes.

Original languageEnglish (US)
Pages (from-to)139-144
Number of pages6
JournalNeuroscience Letters
Volume186
Issue number2-3
DOIs
StatePublished - Feb 17 1995

Keywords

  • Arachidionic acid
  • FCCP
  • Glutamate
  • Hippocampal neurons
  • Intracellular pH
  • Neurotoxicity

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