Activation of α-Latrotoxin Receptors in Neuromuscular Synapses Leads to a Prolonged Splash Acetylcholine Release

The mechanisms of acetylcholine release in presynaptic terminals of motoneurons induced by mutant α-latrotoxin (LTN⁴C) were analyzed. In contrast to wild-type α-latrotoxin that causes both continuous and splash secretion of acetylcholine and necessarity block neuromuscular transmission, LTN⁴C causes...

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Bibliographic Details
Published in:Bulletin of experimental biology and medicine 2009-06, Vol.147 (6), p.701-703
Main Authors: Lelyanova, V. G, Thomson, D, Ribchester, R. R, Tonevitsky, E. A, Ushkaryov, Y. A
Format: Article
Language:English
Subjects:
Acetylcholine - metabolism
acetylcholine release
Animals
Biomedical and Life Sciences
Biomedicine
Biophysics and Biochemistry
Cell Biology
Electrophysiology
Exocytosis
Internal Medicine
Laboratory Medicine
latrophilin
latrotoxin
Mice
Mutation
neuromuscular transmission
Pathology
Receptors, Peptide - metabolism
Receptors, Peptide - physiology
Spider Venoms - genetics
Spider Venoms - metabolism
Synapses - metabolism
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Summary:The mechanisms of acetylcholine release in presynaptic terminals of motoneurons induced by mutant α-latrotoxin (LTN⁴C) were analyzed. In contrast to wild-type α-latrotoxin that causes both continuous and splash secretion of acetylcholine and necessarity block neuromuscular transmission, LTN⁴C causes only splash release lasting over many hours. Thus, activation of α-latrotoxin receptors controls long-lasting enhanced secretion of acetylcholine.
ISSN:0007-4888
1573-8221
DOI:10.1007/s10517-009-0600-5