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Calcium‐Dependent and ‐Independent Acetylcholine Release from Electric Organ Synaptosomes by Pardaxin: Evidence of a Biphasic Action of an Excitatory Neurotoxin
Author(s) -
Arribas Mònica,
Blasi Joan,
Lazarovici Philip,
Marsal Jordi
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.tb03184.x
Subject(s) - neurotoxin , synaptosome , neurotransmitter , acetylcholine , calcium , extracellular , chemistry , lactate dehydrogenase , synaptic vesicle , excitatory postsynaptic potential , biochemistry , biophysics , endocrinology , medicine , biology , vesicle , enzyme , membrane , receptor , organic chemistry
Abstract: The effect of pardaxin, a new excitatory neurotoxin, on neurotransmitter release was tested using purely cholinergic synaptosomes of Torpedo marmorata electric organ. Pardaxin elicited the release of acetylcholine with a biphasic dose dependency. At low concentrations (up to 3 × 10 −7 M ), the release was calcium‐dependent and synaptosomal structure was well preserved as revealed by electron microscopy and measurements of occluded lactate dehydrogenase activity. At concentrations from 3 × 10 −7 M to 10 −5 M , the pardaxin‐induced release of acetylcholine was independent of extracellular calcium, and occluded synaptosomal lactate dehydrogenase activity was lowered, indicating a synaptosomal membrane perturbation. Electron microscopy of 10 −6 M pardaxin‐treated synaptosomes revealed nerve terminals depleted of synaptic vesicles and containing cisternae. At higher toxin concentrations ( 10 −5 M ), there were striking effects on synaptosomal morphology and occluded lactate dehydrogenase activity, suggesting a membrane lytic effect. We conclude that, at low concentrations, this neurotoxin is a promising tool to investigate calcium‐dependent mechanisms of neurotransmitter release in the nervous system.