RGD Reference Report - Severity of alcohol withdrawal symptoms depends on developmental stage of Long-Evans rats. - Rat Genome Database

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Severity of alcohol withdrawal symptoms depends on developmental stage of Long-Evans rats.

Authors: Chung, CS  Wang, J  Wehman, M  Rhoads, DE 
Citation: Chung CS, etal., Pharmacol Biochem Behav. 2008 Apr;89(2):137-44. Epub 2007 Dec 8.
RGD ID: 5129089
Pubmed: PMID:18207224   (View Abstract at PubMed)
PMCID: PMC4134932   (View Article at PubMed Central)
DOI: DOI:10.1016/j.pbb.2007.12.002   (Journal Full-text)

To investigate alcohol dependency and the potential role of age of initial alcohol consumption, Long-Evans (LE) rats were fed an ethanol-containing liquid diet starting at postnatal (P) ages (days): P23-27 (juvenile), P35-45 (adolescent) or P65-97 (young adult). Severity of subsequent withdrawal symptoms was dependent on age when consumption began and on duration of alcohol consumption. Frequency of withdrawal seizures was highest for rats starting consumption as juveniles, intermediate for adolescents and lowest for adults. Normalized to body weight, alcohol consumption was significantly higher for adolescent and juvenile rats than for adults. Sprague-Dawley rats that began alcohol consumption as adolescents (P35) had a level of alcohol consumption identical to that of the adolescent LE rats but showed much lower frequency of withdrawal seizures when tested after 2, 3 and 5 weeks of alcohol consumption. Based on several indicators, the capacity of the juveniles to metabolize ethanol is equal to or exceeds that of adults. Recoveries from a single dose of ethanol (2.5 g ethanol/kg body weight) were faster for juvenile LE rats than adults. The rate of decline in blood ethanol concentration was identical for juvenile and adult rats while the corrected ethanol elimination rate was higher for juveniles. The primary isozyme of alcohol dehydrogenase (ADH) in rat liver, ADH-3, had a similar Km and higher activity in liver preparations from juveniles. In conclusion, LE rats beginning alcohol consumption as juveniles or adolescents develop a severe alcohol withdrawal syndrome that may not be attributed entirely to higher levels of consumption and was not explained by any obvious deficiencies in metabolism.



Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Adh5Ratethanol catabolic process  IDA  RGD 

Molecular Function

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Adh5Ratalcohol dehydrogenase (NAD+) activity  IDA  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Adh5  (alcohol dehydrogenase 5 (class III), chi polypeptide)

Objects referenced in this article
Gene Adh4 alcohol dehydrogenase 4 (class II), pi polypeptide Rattus norvegicus

Additional Information