Abstract
Voltage-activated Ca(2+) channels (VACCs) mediate Ca(2+) influx to trigger action potential-evoked neurotransmitter release, but the mechanism by which Ca(2+) regulates spontaneous transmission is unclear. We found that VACCs are the major physiological triggers for spontaneous release at mouse neocortical inhibitory synapses. Moreover, despite the absence of a synchronizing action potential, we found that spontaneous fusion of a GABA-containing vesicle required the activation of multiple tightly coupled VACCs of variable type.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Analysis of Variance
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Animals
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Calcium / metabolism
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Calcium Channel Blockers
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Calcium Channels / physiology*
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Calcium Channels, N-Type / physiology
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Calcium Channels, P-Type / physiology
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Calcium Channels, Q-Type / physiology
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Cells, Cultured
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Cerebral Cortex / metabolism
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Cerebral Cortex / physiology
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Excitatory Postsynaptic Potentials / physiology
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Mice
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Patch-Clamp Techniques
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Synaptic Transmission / physiology
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Synaptic Vesicles / physiology
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gamma-Aminobutyric Acid / metabolism*
Substances
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Calcium Channel Blockers
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Calcium Channels
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Calcium Channels, N-Type
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Calcium Channels, P-Type
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Calcium Channels, Q-Type
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gamma-Aminobutyric Acid
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Calcium