Electrophysiological evidence against an acetaldehyde role in acute ethanol intoxication /.
| Main Author: | |
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| Other Authors: | , , |
| Format: | Thesis Book |
| Language: | English |
| Published: |
[College Station, Tex.] :
Mikeska,
1978.
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| Subjects: | |
| Online Access: | Link to ProQuest copy Link to OAKTrust copy |
| Abstract: | Some signs of acute ethanol intoxication might result from an action of acetaldehyde, the first metabolite of ethanol degradation in the liver. Support for this concept is derived largely from findings that acetaldehyde can cause behavioral signs and In vitro biochemical effects resembling those caused by ethanol. The present investigation utilized electrophysiological and pharmacological approaches to assess the possibility that acetaldehyde might cause central nervous system signs of ethanol intoxication. To determine if acetaldehyde would cause EEG changes similar to those resulting from ethanol, intravenous injections and infusions of acetaldehyde were made in acutely-prepared rats while recording the spontaneous EEG. Injections and infusions of the aldehyde were also made in rats that were cervlcally-transected or adrenalectomized to determine if the observed EEG effects were the result of a peripheral action of acetaldehyde. To assess the possibility that acetaldehyde-induced EEG changes resulted from an interaction with the catecholamines, injections and infusions of acetaldehyde were made in rats that were pretreated with pargyline or alpha-methyltyrosine (AMT). Finally, a group of experiments was performed to test the hypothesis that ethanol-induced slowing of cerebellar Purkinje-cell firing rate was mediated by acetaldehyde. Ethanol injections were made while recording cerebellar Purkinje-cell activity in two groups of rats, one pretreated with saline and the other pretreated with d-penlcill-amine, a compound that reportedly lowers blood levels of ethanol-derived acetaldehyde. Injections of the lowest acetaldehyde dose (3.125 mg/kg) caused a brief EEG activation (conversion to low voltage, fast activity) which was followed by a return to the normal baseline level of activity. Injections of higher doses (6.25 to 50.0 mg/kg) caused an initial activation followed by a longer period of synchronization (conversion to high voltage, slow activity)... |
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| Item Description: | "Major subject: Zoology." Vita. |
| Physical Description: | x, 137 leaves : illustrations, graphs ; 28 cm |
| Bibliography: | Includes bibliographical references (leaves 70-82). |