Abstract
Before commencing our answer to the question posed in the title, we present a sketch of some required terms and concepts for those unfamiliar with basic neurobiology. The most evident features of a neuron (nerve cell) are a cell body together with a long axon. See Figure 1. Extending from the cell body are a number of finger-like processes called dendrites that usually transmit the input into the cell. The axon branches into many fibres at the end of which are typically located small button-like structures called nerve endings. If the input to a cell is sufficiently excitatory (i. e. if the depolarizing voltage change exceeds a certain threshold) an electrical wave called an action potential is generated, which travels down the axon and passes into each nerve ending. The resulting depolarization brings about the exocytosis (secretion) of special chemicals called neurotransmitters that are believed to be located in spheroidal vesicles (diameter 100–500Å) close to the membrane of the nerve ending at specific release sites. Opposite these sites on the membrane of the adjacent postsynaptic cell is a special active zone with receptors that reversibly bind the released neurotransmitter after it traverses an intercellular gap of width approximately 500Å. The two special release and receptor regions together with the gap constitute a synapse. The average number of vesicles released by an action potential (or by a similar artificial stimulus) is the quantal content, called here total release. Spontaneous release of individual vesicles also occurs, at a low rate.
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H. Arechiga, A. Cannone, H. Parnas and I. Parnas, Blockage of synaptic release by brief hyperpolarizing pulses, J. Physiol. (Lond.) (1990) in press.
J. D. Cooke, K. Okamoto and D. M. J. Quastel, The role of calcium in depolarization-secretion coupling at the motor nerve terminal, J. Physiol (Lond.) 228: 459 (1973).
N. B. Datyner and P. W. Gage, Phasic secretion of acetylcholine at the mammalian neu-romuscular junction, J. Physiol (Lond.) 303: 299 (1980).
B. Hille, Ionic channels in excitable membranes, Sinauer Associates, Sunderland, MA (1984).
B. Hochner, H. Parnas and I. Parnas, Membrane depolarization evokes neurotransmitter release in the absence of calcium entry, Nature 342: 433 (1989).
B. Katz, Nerve, Muscle and Synapse, McGraw-Hill, NY, (1966).
B. Katz and R. Miledi, The role of calcium in neuromuscular facilitation, J. Physiol. (Lond.) 195: 481 (1968).
C. Lustig, Neural transmitter release: models and mechanisms, Ph.D. Thesis, Weizmann Institute of Science (1989).
C. Lustig, H. Parnas and L. Segel, Analysis of spontaneous neurotransmitter release, (1991) unpublished.
E. Neher and A. Marty, Discrete changes of cell membrane capacitance observed under conditions of enhanced secretion in bovine adrenal chromaffin cells, Proc. Nail. Acad. Sci. USA 79: 6712 (1982).
H. Parnas, J. Dudel and I. Parnas, Neurotransmitter release and its facilitation in crayfish. VII. Another voltage dependent process besides Ca entry controls the time course of phasic release, Pflügers Arch. 406: 121 (1986a).
H. Parnas, I. Parnas and L. Segel, A new method for determining cooperativity in neurotransmitter release, J. Theor. Biol. 119: 481 (1986b).
H. Parnas and I. Parnas, The Ca-voltage hypothesis for neurotransmitter release, in: In-tracellular Communication, Theory and Experiment, A. Goldbeter, ed., Academic Press, NY (1989).
H. Parnas and I. Parnas and L. Segel, On the contribution of mathematical models to the understanding of neurotransmitter release, in: International Review of Neurobiology, J. R. Smythies and R. J. Bradley, eds, Acadamic Press: Orlando (1990).
H. Parnas and L. Segel, A theoretical explanation for some effects of calcium on the facilitation of neurotranmitter release, J. Theor. Biol. 91: 125 (1980).
H. Parnas and L. Segel, A theoretical study of calcium entry in nerve terminals, with applications to neurotranmitter release, J. Theor. Biol. 91: 125 (1981).
H. Parnas and L. Segel, Facilitation as a tool to study the entry of calcium and the mechanisms of neurotransmitter release, Progress in Neurobiology 32: 1 (1988).
I. Parnas, J. Dudel and H. Parnas, Neurotransmitter release and its facilitation in crayfish. II. Duration of facilitation and removal processes of calcium from the terminal, Pflügers Arch. 393: 232 (1982a).
I. Parnas and H. Parnas, Calcium is essential but insufficient for neurotransmitter release: the calcium-voltage hypothesis, J. Physiol. (Paris) 81: 289 (1986).
G. H. Prestegard and M. P. O’Brien, Membrane and vesicle fusion, Ann. Rev. Phys. Chem. 38: 383 (1987).
I. Parnas, H. Parnas and Dudel, Neurotransmitter release and its facilitation in crayfish muscle. V. Basis for synapse differentiation of the fast and slow type in one axon, Pflügers Arch. 395: 261 (1982).
R. Rahamimoff, A dual effect of calcium ions on neuromuscular facilitation, J. Physiol. (Lond.) 195: 471 (1968).
A. E. Spruce, L. J. Breckenridge, A. K. Lee and W. Aimers, Properties of the fusion pore that forms during exocytosis of a mast cell secretory vesicle, Neuron 4: 643 (1990).
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Segel, L.A., Parnas, H. (1991). What Controls the Exocytosis of Neurotransmitter?. In: Peliti, L. (eds) Biologically Inspired Physics. NATO ASI Series, vol 263. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9483-0_31
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DOI: https://doi.org/10.1007/978-1-4757-9483-0_31
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