descriptionPublicationkeyboard_double_arrow_right Article 01 Sep 1999 English Publisher:Springer Science and Business Media LLCJournal:Nature Neuroscience, volume 2, pages 785-790 (issn: 1097-6256, eissn: 1546-1726,

Authors: Maureen W. McEnery; Seema Gupta; Stephanie Schorge; Zhixin Lin; Zhixin Lin; Diane Lipscombe;

doi: 10.1038/12153

pmid: 10461216

Calcium channel activation stabilizes a neuronal calcium channel mRNA

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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.

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Keywords

Neurons, Calcium Channels, L-Type, Transcription, Genetic, Action Potentials, Superior Cervical Ganglion, Calcium Channel Blockers, Membrane Potentials, Rats, Gene Expression Regulation, omega-Conotoxin GVIA, Animals, Nimodipine, Calcium Channels, Nerve Growth Factors, RNA, Messenger, Peptides, 3' Untranslated Regions, Cells, Cultured

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