Premium
Cerebral Metabolic State During the Ethanol Withdrawal Reaction in the Rat
Author(s) -
Hemmingsen R.,
Chapman A. G.
Publication year - 1980
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1980.tb11244.x
Subject(s) - phosphocreatine , medicine , ketone bodies , endocrinology , glycogen , ethanol , chemistry , energy charge , adenylate kinase , creatine , cerebral cortex , adenine nucleotide , metabolism , biochemistry , energy metabolism , nucleotide , enzyme , gene
A severe ethanol withdrawal reaction was induced in rats by means of repeated intragastric intubation during a 4‐day period. At the peak of the withdrawal reaction cerebral cortical tissue was frozen in situ for analysis of glycogen, glucose, phosphocreatine, creatine, ATP, ADP, AMP, lactate, pyruvate, GAB A, β‐hydroxybutyrate, acetoacetate, cAMP and cGMP. Blood glucose concentration was also measured. The level of brain glycogen was decreased during ethanol withdrawal. Brain glucose concentration was increased, probably secondary to the increase in blood glucose concentration. The calculated NADH/NAD + ratio was slightly increased during the withdrawal and brain ATP concentration and adenine nucleotide pool size were decreased. The adenylate energy charge remained unchanged. The overall changes in the metabolites were in agreement with the previously shown metabolic activation during ethanol withdrawal. The brain concentrations of ketone bodies (β‐hydroxybutyrate and acetoacetate) during withdrawal did not deviate from controls, indicating that no abnormal ketone metabolism had developed as a consequence of the long‐lasting ethanol intoxication. No changes were observed in the concentrations of GABA, cAMP, or cGMP in the rat cerebral cortex during ethanol withdrawal.