Abstract
L-type calcium channels play only a minor role in basal neurotransmitter release in brain neurons but contribute significantly after induction of plasticity. Very little is known about mechanisms that enable L-type calcium channel participation in neurotransmitter release. Here, using mouse primary cortical neurons, we found that inhibition of Erk1/2 (extracellular signal-regulated kinases 1 and 2) enhanced synaptic vesicle exocytosis by increasing calcium influx through L-type calcium channels. Furthermore, inhibition of Erk1/2 increased the surface fraction of these channels. These findings indicate a novel inhibitory effect of Erk1/2 on synaptic transmission through L-type calcium channels.
Publication types
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Research Support, N.I.H., Intramural
MeSH terms
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Animals
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Axons / physiology
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Calcium / metabolism
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Calcium Channels, L-Type / physiology*
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Cells, Cultured
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Cerebral Cortex / cytology
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Cerebral Cortex / physiology
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DNA / genetics
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Electric Stimulation
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Endocytosis / physiology
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Exocytosis / physiology*
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Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors
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Extracellular Signal-Regulated MAP Kinases / physiology*
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Female
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Fluorescent Antibody Technique
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Image Processing, Computer-Assisted
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Mice
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Mice, Inbred C57BL
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Mitogen-Activated Protein Kinases / antagonists & inhibitors
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Neuronal Plasticity / drug effects
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Neuronal Plasticity / physiology
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Pregnancy
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Synaptic Vesicles / physiology*
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Transfection
Substances
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Calcium Channels, L-Type
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DNA
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Extracellular Signal-Regulated MAP Kinases
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Mitogen-Activated Protein Kinases
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Calcium