Abstract
Ethanol withdrawal enhances the current density of calcium (Ca(2+)) channels in inferior colliculus (IC) neurons. The present report shows that ethanol withdrawal markedly enhanced the susceptibility to seizures as it decreased significantly the protein levels of alpha(1B) subunit associated with N-type Ca(2+) channel in IC neurons of animals not tested for seizures. Thus, remodeling of N-type Ca(2+) channels may play an important role in neuronal hyperexcitability that leads to ethanol withdrawal seizures.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Alcohol-Induced Disorders, Nervous System / metabolism*
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Alcohol-Induced Disorders, Nervous System / physiopathology
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Animals
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Calcium Channels, N-Type / drug effects*
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Calcium Channels, N-Type / metabolism
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Calcium Signaling / drug effects
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Calcium Signaling / physiology
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Disease Models, Animal
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Down-Regulation / drug effects*
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Down-Regulation / physiology
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Inferior Colliculi / drug effects*
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Inferior Colliculi / metabolism
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Inferior Colliculi / physiopathology
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Male
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Membrane Potentials / drug effects
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Membrane Potentials / physiology
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Neurons / drug effects*
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Neurons / metabolism
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Rats
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Rats, Sprague-Dawley
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Substance Withdrawal Syndrome / metabolism*
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Substance Withdrawal Syndrome / physiopathology
Substances
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Cacna1b protein, mouse
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Calcium Channels, N-Type