Abstract
We have identified a calcium-dependent pathway in neurons that regulates expression levels of the alpha1B subunit and N channel current. When neurons are depolarized and voltage-gated calcium channels activated, the half-life of cellular N channel alpha1B mRNA is prolonged. This stabilizing effect of depolarization is mediated through the 3' untranslated region of a long form of the alpha1B mRNA and may represent a form of modulation of N-channel levels that does not require changes in gene transcription. Increases in N channel expression would affect several key neuronal functions controlled by calcium, including transmitter release and neurite outgrowth.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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3' Untranslated Regions / genetics
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Action Potentials / physiology
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Animals
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Calcium Channel Blockers / pharmacology
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Calcium Channels / genetics*
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Calcium Channels / physiology*
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Calcium Channels, L-Type
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Cells, Cultured
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Gene Expression Regulation*
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Membrane Potentials
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Nerve Growth Factors / pharmacology
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Neurons / drug effects
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Neurons / physiology*
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Nimodipine / pharmacology
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Peptides / pharmacology
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RNA, Messenger / genetics
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RNA, Messenger / metabolism*
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Rats
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Superior Cervical Ganglion / physiology*
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Transcription, Genetic
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omega-Conotoxin GVIA
Substances
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3' Untranslated Regions
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Calcium Channel Blockers
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Calcium Channels
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Calcium Channels, L-Type
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Nerve Growth Factors
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Peptides
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RNA, Messenger
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Nimodipine
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omega-Conotoxin GVIA