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Calcium Transport and the Release of Neurotransmitters: Effects of Drugs in Vivo and in Vitro

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Regulatory Mechanisms of Synaptic Transmission

Abstract

The role of calcium ions in neurotransmitter release is now amply recognized. External calcium appears to enter the presynaptic terminal upon depolarization, and the increase in its intraterminal cytoplasmic concentration somehow induces the release of the neurotransmitter (21,25,26,39,40,51). In vertebrates this phenomenon occurs both at neuromuscular junctions, where the release of acetylcholine (ACh) occurs probably from synaptic vesicles, and in central synapses, where the role of vesicles is less clear. Thus, in several preparations from mammalian central nervous system, such as tissue slices or synaptosomes, it has been shown that the depolarization-induced release of catecholamines (6,10), ACh (8,45,64) or neurotransmitter amino acids such as GABA (10,16,27,44,56), glutamate (9,53) or glycine (27,44) is a phenomenon dependent on the presence of external Ca2+. Because of this necessity for Ca2+ transport across the presynaptic membrane in order to induce transmitter release, drugs capable of modifying Ca2+ transport should affect the release of neurotransmitters. This approach has been followed in the present communication in two different ways: 1) drugs which block Ca2+ transport or apparently increase its cytoplasmic concentration at the nerve terminals have been injected to experimental animals, and 2) the effect of such drugs on neurotransmitter release has been studied in synaptosomes prepared from brain tissue.

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Tapia, R., Arias, C. (1981). Calcium Transport and the Release of Neurotransmitters: Effects of Drugs in Vivo and in Vitro. 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_9

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  • DOI: https://doi.org/10.1007/978-1-4684-3968-7_9

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