Effects of lactic acidosis on the function of cerebral cortical synaptosomes

Elizabeth White, Henryk Juchniewicz, John Clark

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)


Synaptosomes exposed to anoxic insult produce lactate at a slow rate (measured over 60 min). No measurable damaging effects were produced by prolonged depolarisation, anoxic insult, or exogenous lactate (2–32 mM) either on the synaptic plasma membrane (as judged by release of lactate dehydrogenase and soluble proteins), or on synaptosomal phospholipases (as judged by choline release from membrane phospholipids). Potassium‐stimulated acetylcholine release was decreased by incubation in the presence of lactate (2–32 mM), as was potassium‐ and veratrine‐stimulated calcium uptake and the calcium content of depolarised synaptosomes. The intrasynaptosomal pH was also reduced but there was no stimulation of oxygen radical production (as judged by H2O2 generation) by exogenous lactate. The role that lactic acidosis may play in giving rise to the altered calcium homeostasis and decreased acetylcholine release from synaptosomes exposed to anoxic insult is discussed.
Original languageEnglish
Pages (from-to)154-161
Number of pages8
JournalJournal of Neurochemistry (JNC)
Issue number1
Publication statusPublished - Jan 1989


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