Calcium-induced modulation of synaptic transmission
Autor: | P. D. Bregestovski, L. G. Khaspekov |
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Rok vydání: | 2007 |
Předmět: | |
Zdroj: | Biochemistry (Moscow) Supplement Series A: Membrane and Cell Biology. 1:28-37 |
ISSN: | 1990-7494 1990-7478 |
DOI: | 10.1134/s1990747807010035 |
Popis: | Calcium (Ca2+) is a second messenger regulating a wide variety of intracellular processes. Using GABA-and glycinergic synapses as examples, this review analyzes two functions of this unique ion: postsynaptic Ca2+-dependent modulation of receptor-operated channels and Ca2+-induced retrograde regulation of neurotransmitter release from the presynaptic terminals. Phosphorylation, rapid Ca2+-induced modulation via intermediate Ca2+-binding proteins, and changes in the number of functional receptors represent the main pathways of short-and long-term plasticity of postsynaptic receptor-operated channel machinery. Retrograde signaling is an example of synaptic modulation triggered by stimulation of postsynaptic cells and mediated via regulation of presynaptic neurotransmitter release. This mechanism provides postsynaptic neurons with efficient tools to control the presynaptic afferents in an activity-dependent mode. Elevation of intracellular Ca2+ in a postsynaptic neuron triggers the synthesis of endocannabinoids (derivatives of arachidonic acid). Their retrograde diffusion through the synaptic cleft and consequent activation of presynaptic G-protein coupled to CB1 receptors inhibits the release of neurotransmitter. These mechanisms of double modulation, which include control over the function of postsynaptic ion channels and retrograde suppression of the release machinery, play an important role in Ca2+-dependent control of the main excitatory and inhibitory synaptic pathways in the mammalian nervous system. |
Databáze: | OpenAIRE |
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