ABSTRACT
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.
Subject(s)
Acetylcholine/metabolism , Receptors, Peptide/metabolism , Receptors, Peptide/physiology , Synapses/metabolism , Animals , Electrophysiology , Exocytosis , Mice , Mutation , Spider Venoms/genetics , Spider Venoms/metabolismABSTRACT
Latrophilin 1 (presynaptic receptor) binds α-latrotoxin from black widow spider venom and regulates neurotransmitter release from nerve endings. The study of the mechanism of action of this receptor is impeded by the existence of closely related latrophilins 2 and 3. A profile of differences detecting the most differing and identical sites in several proteins was developed in order to obtain highly specific antibodies for differentiation between isoforms of related proteins. In addition, we used an algorithm for prediction of immunogenic sites of the protein, based on the basic vector method. The peptides selected using this algorithm were used for immunization of animals. The resultant sera exhibited the estimated specificity and high affinity for the corresponding receptor forms.
