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KMID : 0604620010080010001
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Dongguk Journal of Medicine
2001 Volume.8 No. 1 p.1 ~ p.28
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Presynaptic Plastictiy: The Role of Neuronal Activity in Modulation of of Ca²^(+) -Dependent Transmitter Release
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Hong Sungwon
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Abstract
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Differences in impulse activity appear to be involved in the differentiation of transmitter releasing properties at the axonterminals in both vertebrates and inverteb-These differences in transmitter release appear to result largely from differences in the density of Ca^(2+) channels at the active zone. Since specific types, of voltage-dependent Ca^(2+) channels can be selectively modulated by voltage and Ca^(2+)influx, activity-dependent modulation of Ca ^(2+), channels likely control the evoked-release of transmitter. Voltage- and Ca^(2+)-dependent inactivations of Ca^(2+) channel are more documented and widespread than voltage-dependent facilitation. There indirect evidence for the involvement of Ca^(2+) channel inactivation in short-term depression in transmitter release. In addition, there is evidence that Ca^(2+) -dependent reduction in Ca^(2+) current is involved in long-term depression at crustacean neuromuscular junction. The reduction in Ca^(2+) current apparently result from a reduction in the number of functional Ca^(2+) channels. The mechanism of this change may include Ca^(2+) channel internalization as well as decreased Ca^(2+) channel synthesis. A more direct examination of Ca^(2+) current at synaptic terminals will be necessary to confirm these findings. The activity-dependent modulation of Ca^(2+) current could play a role in the development of Ca^(2+) current density at synaptic terminals and subsequently synaptic plasticity.
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KEYWORD
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