Regulation of acetylcholine liberation from presynaptic nerve terminals.
Acetylcholine is liberated from motor nerve terminals either as a molecular leakage or as quantal packages; the latter form of release is responsible for signaling across the neuromuscular synapse. Three main factors determine the number of quanta liberated by the nerve impulse: the degree of presynaptic depolarisation, the frequency of activation of the nerve terminal, and calcium ion concentration in the extracellular medium. These factors seem to act yb changing the free calcium ion concentration [Ca]in in the presynaptic nerve terminal. Thus, processes that change [Ca]in will determine efficiency of synaptic transmission. These processes include fluxes of calcium ions across the presynaptic membrane and reversible translocation by intracellular organelles such as mitochondria, vesicles and soluble molecules. The level of intracellular [Ca] can be changed by ion-containing liposomes. One of the main physiological determinants of the level of transmitter release is potentiation, where the increase in transmitter release is caused by transmembranal processes and intracellular translocation.
D000109:Acetylcholine / Q000378:metabolism*; D000200:Action Potentials; D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology; D003600:Cytosol / Q000378:metabolism; D004721:Endoplasmic Reticulum / Q000378:metabolism; D007473:Ion Channels / Q000502:physiology; D008928:Mitochondria / Q000378:metabolism; D009046:Motor Neurons / Q000187:drug effects / Q000378:metabolism*; D009119:Muscle Contraction; D009469:Neuromuscular Junction / Q000502:physiology; D011898:Ranidae; D012964:Sodium / Q000378:metabolism; D013569:Synapses / Q000187:drug effects / Q000378:metabolism*
D007473:Ion Channels; D012964:Sodium; D000109:Acetylcholine; D002118:Calcium