Abstract
Complexins (Cplxs) are key regulators of synaptic exocytosis, but whether they act as facilitators or inhibitors is currently being disputed controversially. We show that genetic deletion of all Cplxs expressed in the mouse brain causes a reduction in Ca(2+)-triggered and spontaneous neurotransmitter release at both excitatory and inhibitory synapses. Our results demonstrate that at mammalian central nervous system synapses, Cplxs facilitate neurotransmitter release and do not simply act as inhibitory clamps of the synaptic vesicle fusion machinery.
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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Adaptor Proteins, Signal Transducing
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Adaptor Proteins, Vesicular Transport
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Animals
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Brain / metabolism
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Brain / physiology
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Calcium / metabolism*
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Calcium / pharmacology
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Evoked Potentials
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Exocytosis* / genetics
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Eye Proteins / genetics
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Eye Proteins / physiology*
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Mice
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Mice, Knockout
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Nerve Tissue Proteins / genetics
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Nerve Tissue Proteins / metabolism*
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Nerve Tissue Proteins / physiology*
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Neuronal Plasticity
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Neurons / metabolism
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Neurons / physiology
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Neurotransmitter Agents / metabolism*
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Synapses / metabolism*
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Synaptic Transmission
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Synaptic Vesicles / drug effects
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Synaptic Vesicles / metabolism
Substances
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Adaptor Proteins, Signal Transducing
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Adaptor Proteins, Vesicular Transport
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Cplx3 protein, mouse
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Eye Proteins
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Nerve Tissue Proteins
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Neurotransmitter Agents
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complexin I
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complexin II
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Calcium