Abstract
The ubiquitous role of calcium in ethanol actions measured electrophysiologically in central neurons is discussed. Acute ethanol administration to rat hippocampal neurons in vitro causes a hyperpolarization, increased AHPs, increased EPSPs and IPSPs, decreased modelled electronic interneuronal coupling, decreased high threshold Ca2+ currents, increased Ik, and increased synaptic GABAA currents. Alcohol withdrawal reverses some of these actions. Ca2+ is implicated in all of the above ethanol mediated effects.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Calcium / metabolism*
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Electrophysiology
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Ethanol / toxicity*
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Hippocampus / drug effects*
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Hippocampus / metabolism*
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Homeostasis
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In Vitro Techniques
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Male
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Neurons / drug effects
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Neurons / metabolism
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Potassium Channels / drug effects
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Potassium Channels / metabolism
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Rats
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Receptors, GABA-A / drug effects
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Receptors, GABA-A / metabolism
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Synaptic Transmission / drug effects
Substances
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Potassium Channels
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Receptors, GABA-A
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Ethanol
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Calcium