Abstract
Publisher Summary Modulation of acetylcholine (ACh) release is of physiological and pharmacological importance. In order to consider its molecular aspects, the existence of vesicular and extravesicular ACh pools should be taken into account. To disclose molecular mechanisms underlying neurotransmitter release, protein composition of synaptic vesicles as well as their individual participation in synaptic vesicle movement toward the active zone, in docking and fusion with the plasma membrane and in exocytotic pore formation is all essential. In the release of vesicular ACh, phosphorylation-dephosphorylation of certain proteins plays a major role. In ACh release, a triggering role for Ca 2+ has been demonstrated. In addition, Ca 2+ -independent ACh release that is probably extravesicular, has also been documented. Vesicular ACh release seems to correlate with quanta1 release, triggered by Ca 2+ , whereas extravesicular ACh release may be Ca 2+ -independent and non-quanta1 in nature. Since the latter is enhanced by ouabain, Na + , K + -ATPase seems to be involved in this process. Finally, the participation of auto-, homo-, and hetero-receptors in the modulation of ACh release has been widely recognized.
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