Activation of alpha-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 alpha-latrotoxin (LT(N4C)) were analyzed. In contrast to wild-type alpha-latrotoxin that causes both continuous and splash secretion of acetylcholine and necessarity block neuromuscular transmission, LT(N4C) causes only splash release lasting over many hours. Thus, activation of alpha-latrotoxin receptors controls long-lasting enhanced secretion of acetylcholine.
Lelyanova
V G
VG
Department of Cell and Molecular Biology, Imperial College, London, U.K.
Thomson
D
D
Ribchester
R R
RR
Tonevitsky
E A
EA
Ushkaryov
Y A
YA
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D004594:Electrophysiology; D005089:Exocytosis; D051379:Mice; D009154:Mutation; D018000:Receptors, Peptide / Q000378:metabolism* / Q000502:physiology*; D013111:Spider Venoms / Q000235:genetics / Q000378:metabolism; D013569:Synapses / Q000378:metabolism*
D018000:Receptors, Peptide; D013111:Spider Venoms; C034800:alpha-latrotoxin receptor; C020763:alpha-latrotoxin; D000109:Acetylcholine