Abstract
We investigated the effect of chronic nicotine administration on high voltage-gated calcium channels (HVCCs) in the mouse cerebral cortex. The treatment significantly increased expression of alpha1C, alpha1D, alpha1F, and alpha2/delta1 subunits with no changes of beta4 subunit of L-type HVCCs. [(3)H]Diltiazem binding to the particulate fractions increased with increased Bmax value. These results indicate that chronic nicotine treatment up-regulates L-type HVCCs, which is due to increased expression of alpha1 and alpha2/delta1 subunits.
Publication types
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Comparative Study
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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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Blotting, Western / methods
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Calcium Channel Blockers / pharmacokinetics
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Calcium Channels, L-Type / genetics
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Calcium Channels, L-Type / metabolism*
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Cerebral Cortex / drug effects*
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Diltiazem / pharmacokinetics
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Dose-Response Relationship, Drug
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Drug Administration Schedule
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Drug Interactions
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Gene Expression / drug effects*
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Male
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Mecamylamine / pharmacology
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Mice
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Nicotine / administration & dosage*
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Nicotinic Agonists / administration & dosage*
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Nicotinic Antagonists / pharmacology
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Protein Subunits / genetics
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Protein Subunits / metabolism
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Tritium / pharmacology
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Up-Regulation / drug effects
Substances
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Calcium Channel Blockers
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Calcium Channels, L-Type
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Nicotinic Agonists
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Nicotinic Antagonists
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Protein Subunits
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Tritium
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Mecamylamine
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Nicotine
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Diltiazem