Abstract
Ethanol has central serotonergic effects that may be of pathogenetic importance in a subgroup of alcohol-dependent patients with a central serotonergic hypofunction. Recent results indicate that pronounced amplitude increases of auditory evoked responses (tangential dipoles, N1/P2 component) with increasing stimulus intensity (loudness) may be an indicator of such a low serotonergic neurotransmission. Because of its serotonin-agonistic effects, ethanol can be expected to decrease this intensity dependence. Twenty-eight alcoholic patients were studied both in the intoxication phase and after 1 week of withdrawal. A reduced intensity dependence of the tangential dipole activity was observed in the intoxicated state. Correspondingly, a reduction of this parameter was found in 14 healthy subjects after an ethanol load (1 g/kg, p.o.).
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adult
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Aged
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Alcohol Withdrawal Delirium / physiopathology
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Alcohol Withdrawal Delirium / psychology
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Alcoholic Intoxication / physiopathology*
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Alcoholic Intoxication / psychology
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Alcoholic Intoxication / rehabilitation
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Alcoholism / physiopathology*
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Alcoholism / psychology
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Alcoholism / rehabilitation
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Arousal / drug effects
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Arousal / physiology
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Biomarkers
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Brain / drug effects
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Brain / physiopathology
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Brain Mapping
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Electroencephalography / drug effects
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Ethanol / administration & dosage
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Ethanol / pharmacokinetics
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Evoked Potentials, Auditory / drug effects*
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Evoked Potentials, Auditory / physiology
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Female
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Humans
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Male
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Middle Aged
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Neurologic Examination
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Receptors, Serotonin / drug effects*
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Receptors, Serotonin / physiology
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Reference Values
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Serotonin / physiology*
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Signal Processing, Computer-Assisted
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Transferrin / analogs & derivatives
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Transferrin / metabolism
Substances
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Biomarkers
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Receptors, Serotonin
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Transferrin
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carbohydrate-deficient transferrin
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Serotonin
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Ethanol