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On the Role of Mitochondria in Neurotransmitter Release

  • Chapter
Regulatory Mechanisms of Synaptic Transmission

Abstract

Depolarization of the presynaptic membrane and the presence of calcium ions in the extracellular medium appear to be essential to evoke transmitter release under physiological conditions. Most probably depolarization of the nerve terminal causes an increase in the membrane Ca2+ conductance and Ca2+ flow inside the presynaptic nerve ending along their electrochemical gradient. However depolarization is not necessary to evoke transmitter liberation since procedures that elicit an increased intracellular calcium ([Ca++]i) in the absence of depolarization lead to transmitter liberation. Thus, direct calcium injection into the squid axon and calcium entry facilitated by the calcium ionophore A23187 in synaptosomes, induce an increased transmitter release (22,31,40,46,48). This indicates that an elevated [Ca++] i is essential for transmitter release. At the frog neuromuscular junction spontaneous quantal release can be detected at rest and this rate of release is less dependent on extracellular calcium than evoked transmitter release (38,39). However, treatments that enhance [Ca++] i cause an increase in spontaneous transmitter liberation.

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Sandoval, M.E. (1981). On the Role of Mitochondria in Neurotransmitter Release. In: Tapia, R., Cotman, C.W. (eds) Regulatory Mechanisms of Synaptic Transmission. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-3968-7_10

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  • DOI: https://doi.org/10.1007/978-1-4684-3968-7_10

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