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Effect of α‐Latrotoxin on Acetylcholine Release and Intracellular Ca 2+ Concentration in Synaptosomes: Na + ‐Dependent and Na + ‐Independent Components
Author(s) -
Deri Z.,
Bors P.,
AdamVizi Vera
Publication year - 1993
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1993.tb03255.x
Subject(s) - divalent , acetylcholine , chemistry , choline , biophysics , synaptosome , intracellular , depolarization , sodium , extracellular , calcium , membrane , efflux , biochemistry , endocrinology , biology , organic chemistry
We studied the effect of α‐latrotoxin (αLTX) on [ 14 C]acetylcholine ([ 14 C]ACh) release, intracellular Ca 2+ concentration ([Ca 2+ ] i ), plasma membrane potential, and high‐affinity choline uptake of synaptosomes isolated from guinea pig cortex. αLTX (10 −10 ‐10 −8 M ) caused an elevation of the [Ca 2+ ] i as detected by Fura 2 fluorescence and evoked [ 14 C]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 [Ca 2+ ] i and [ 14 C]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 [Ca 2+ ] i and [ 14 C]ACh release remained in the absence of Na + . Both the Na + ‐dependent and the Na + ‐independent components of the αLTX‐evoked [ 14 C]ACh release partly required the presence of either Mg 2+ or Ca 2+ . The nonneurotransmitter [ 14 C]choline was released along with [ 14 C]ACh, but this release did not depend on the presence of either Na + or Ca 2+ , 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.