The Involvement of Alkaline Earth Cations in the Control of Acetylcholine Release
Neuroscientists allured by the mechanisms of transmitter secretion have at their disposal fortuitous electrophysiological deflections which allow a direct, moment to moment assay for acetylcholine (ACh) secretion. Specifically, the ratio of the amplitudes of the electrical events associated with neurally-evoked ACh release (end-plate potentials, EPFs) to the spontaneous potentials (miniature end-plate potentials, MEPPs) serves as a reliable estimate of the mean number of ACh quanta released synchronously by a nerve impulse (M, del Castillo and Katz, 1954). Extracellular Ca ions are essential for the process of evoked ACh release (for reviews see Katz, 196?; Silinsky, 1985). Specifically Ca must be equlibrated with a receptor near the external surface of the calcium channel prior to depolarization to support transmitter secretion. Depolarization, normally provided by the action potential, opens these voltage-sensitive calcium channels and Ca enters the nerve terminal cytoplasm down its electrochemical gradient. Once in the cytoplasm, Ca reduces a series of energy barriers and promotes ACh release.
KeywordsSynaptic Vesicle Transmitter Release Motor Nerve Terminal Transmitter Secretion MEPP Frequency
Unable to display preview. Download preview PDF.
- Augustine, G.J., andEckert, R,, 1984, Divalent cations differentially support transmitter release at the squid giant synapse, J. Physiol. (London), 346: 257.Google Scholar
- del Castillo, J., and Katz, B., 1954, Quantal components of the end-plate potential. J. Physiol. (London), 124: 560.Google Scholar
- Heuser, J.E., 1977, Synaptic vesicle exocytosis revealed i n quick-frozen frog neuromuscular junctions treated with 4-aminopyridi ne and given a single electrical shock, in: “Approaches to the Cell Biology of Neurons” W.M. Cowan, and J.A. Ferrendelli eds., Society for Neurosciences Symposium, Volume 2.Google Scholar
- Katz, B., 1969, “The Release of Neural Transmitter Substances” The Sherrington Lectures X. Liverpool University Press, Liverpool, U.K.Google Scholar
- Kharasch, E.D., Mellow, A.M., and Silinsky, E.M.,1981, Intracellular magnesium does not antagonize calcium-dependent acetylcholine secretion. J. Physiol. (London), 314: 255.Google Scholar
- Lang, B., Newsome-Davi s, J., Prior, C.,and Wray, D., 1984, Effect of passively transferred Lambert-Eaton myasthenic syndrome antibodies on the calcium sensitivity of transmitter release in the mouse. J. Physiol. (London), 357: 28 P.Google Scholar
- Meiri, U., and Rahamimoff, R., 1971, Activation of transmitter release by strontium and calcium ions at the neuromuscular junction. J. Physiol. (London), 215: 709.Google Scholar
- Mellow, A.M., Perry, B.D., and Silinsky, E.M., 1982, Effects of calcium and strontium in the process of acetylcholine release from motor nerve endings. J. Physiol. (London), 328: 547.Google Scholar
- Silinsky, E.M., 1977, Can barium support the rei ease of acetylcholine by nerve impulses? Brit. J. Pharmacol., 59: 215.Google Scholar
- Silinsky, E.M., 1978, On the role of barium in supporting the asynchronous release of acetylcholine quanta by motor nerve impulses. J. Physiol. (London), 274: 157.Google Scholar
- Silinsky, E.M., 1981, On the calcium receptor that mediates depolarization- secretion coupling at cholinergic motor nerve terminals. Brit. J. Pharmacol., 73: 413.Google Scholar
- Silinsky, E.M., 1986, Inhibition of transmitter release by adenosine: Are calcium currents depressed or are the intracellular effects of calcium impaired? Trends. Pharmacol. Sci., 6:(in press).Google Scholar