Effect of α‐Latrotoxin on Acetylcholine Release and Intracellular Ca2+ Concentration in Synaptosomes: Na+‐Dependent and Na+‐Independent Components

Z. Deri, P. Bors, Vera Adam‐Vizi

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30 Citations (Scopus)


Abstract: We studied the effect of α‐latrotoxin (αLTX) on [14C]acetylcholine ([14C]ACh) release, intracellular Ca2+ concentration ([Ca2+]i), plasma membrane potential, and high‐affinity choline uptake of synaptosomes isolated from guinea pig cortex. αLTX (10−10‐10−8M) caused an elevation of the [Ca2+]i as detected by Fura 2 fluorescence and evoked [14C]ACh efflux. Two components in the action of the toxin were distinguished: one that required the presence of Na+ in the external medium and another that did not. Displacement of Na+ by sucrose or N‐methylglucamine in the medium considerably decreased the elevation of [Ca2+]i and [14C]ACh release by αLTX. The Na+‐dependent component of the αLTX action was obvious in the inhibition of the high‐affinity choline uptake of synaptosomes. Some of the toxin action on both [Ca2+]i and [14C]ACh release remained in the absence of Na+. Both the Na+‐dependent and the Na+‐independent components of the αLTX‐evoked [14C]ACh release partly required the presence of either Mg2+ or Ca2+. The nonneurotransmitter [14C]choline was released along with [14C]ACh, but this release did not depend on the presence of either Na+ or Ca2+, indicating nonspecific leakage through the plasma membrane. We conclude that there are two factors in the release of ACh from synaptosomes caused by the toxin: (1) cation‐dependent ACh release, which is related to (a) Na+‐dependent divalent cation entry and (b) Na+‐independent divalent cation entry, and (2) nonspecific Na+‐ and divalent cation‐independent leakage.

Original languageEnglish
Pages (from-to)1065-1072
Number of pages8
JournalJournal of neurochemistry
Issue number3
Publication statusPublished - Mar 1993


  • Acetylcholine release
  • Choline efflux
  • Choline uptake
  • Na dependence
  • α‐Latrotoxin

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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