Phenytoin ameliorates the memory deficit induced in the young chick by ethanol toxicity in association with thiamine deficiency.
The experiments reported in this series of studies demonstrate that thiamine deficiency, induced pharmacologically by oxythiamine (OT) coupled with the acute administration of ethanol can adversely affect memory processing in the young chick. The interaction between the avitaminosis and ethanol neurotoxicity exerted its effects through the inhibition of the development of the intermediate (ITM) stage of memory (i.e., following 10 min after training), consequently affecting development of the long-term stage of memory and leaving the short-term memory stage intact. The amnesic effect of OT-induced thiamine deficiency and exposure to alcohol was ameliorated by the administration of phenytoin [diphenylhydantoin (DPH)] immediately following the training experience. As the ITM stage of memory has been suggested to rely on the activities of Na(+)/K(+) ATPase, and as DPH is a facilitator of Na(+)/K(+) ATPase activity amongst its other actions, it may be that the combined effect of OT and ethanol exposure is by interfering with Na(+)/K(+) ATPase activity, thus undermining the expression and maintenance of the memory in the period from 10 min following aversant training.[1]References
- Phenytoin ameliorates the memory deficit induced in the young chick by ethanol toxicity in association with thiamine deficiency. Crowe, S.F., El-Hadj, D. Pharmacol. Biochem. Behav. (2002) [Pubmed]
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