Abstract
Previous studies of neuromuscular synapses in mammals have detected metabotropic cholinoreceptors (mChR) and GABA receptors. Activation of both types of receptor leads to changes in the intensity of calcium-dependent quantum release of acetylcholine (ACh). We report here studies using recording of calcium signals (Ca2+ transients) to assess changes in calcium levels in motor nerve endings on application of the ligands of various receptors. Muscarine (an mChR agonist) was found to decrease the amplitude of the calcium transient, while atropine (an mChR blocker), conversely, led to an increase in the signal. Application of GABA had no effect on the parameters of the transient. Thus, the mechanism of regulation of mChR-triggered ACh neurosecretion may be mediated by changes in the calcium level in nerve terminals, while the effect of GABA on the process of ACh neurosecretion is mediated by molecular mechanisms not linked directly with calcium metabolism in the motor terminal.
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