ABSTRACT
Experiments on neuromuscular synapses of rats at different stages of ontogenesis have been performed. It has been found that one of the reasons of higher asynchrony of the release of single quanta of acetylcholine in the synapses of newborn animals is the activity of the presynaptic dihydropyridine-sensitive calcium channels of the L-type.
Subject(s)
Acetylcholine/metabolism , Calcium Channels, L-Type/physiology , Ion Channel Gating/physiology , Neuromuscular Junction/physiology , Neurotransmitter Agents/metabolism , Synaptic Transmission/physiology , Animals , Animals, Newborn , Calcium Channel Blockers/administration & dosage , Calcium Channels, L-Type/drug effects , Dihydropyridines/administration & dosage , Dose-Response Relationship, Drug , In Vitro Techniques , Ion Channel Gating/drug effects , Neurogenesis/physiology , Neuromuscular Junction/drug effects , Rats , Rats, Wistar , Synaptic Transmission/drug effectsABSTRACT
The effects of calcium on the quantal content of nerve-evoked endplate currents (EPC) and on the temporal parameters of quantal release were studied in the frog neuromuscular synapse using the method of "subtractions". It was shown that under physiological conditions quanta generating multiquantal postsynaptic responses were released nonsynchronously because of a considerable variability of latencies of the uniquantal responses forming multiquantal EPC. Different calcium dependences for EPCs quantal content and time course of the quantal release were revealed. The average quantal content grew exponentially with the increase in calcium concentration from 0.4 to 1.8 mmol/L, whereas the release synchronicity reached the maximum at 1 mmol/L calcium. It was suggested that the changes in the synchronicity of the evoked release were one of the mechanisms of the synaptic plasticity.
