Proto-oncogene c-fos induction in thiamine-deficient encephalopathy. Protective effects of nicardipine on pyrithiamine-induced lesions.

Abstract

Treatment of rats with the central thiamine antagonist, pyrithiamine, results in severe neurological symptoms such as ataxia and convulsions. Induction of proto-oncogene c-fos expression, often related to seizure activity, has been detected in the brains of thiamine-deficient rats by means of Northern blot analysis and in situ hybridization. Region-selective increases of lactate observed following thiamine deficiency development are largely coincident with histologically vulnerable regions. When thiamine-deficient rats were treated with the calcium channel blocker, nicardipine, lesions associated with thiamine deficiency did not appear and there was no induction of c-fos mRNA expression. This suggests a neurocytoprotective role of nicardipine to neuronal cell damage in thiamine-deficient encephalopathy.

• Authors: P Munujos, M Vendrell, I Ferrer
• Journal: Journal of the neurological sciences (J Neurol Sci) Vol. 118 Issue 2 Pg. 175-80 (Sep 1993) ISSN: 0022-510X [Print] Netherlands
• PMID: 8229066 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Lactates
• Oligonucleotide Probes
• Pyrithiamine
• Nicardipine

Topics

• Animals
• Female
• Gene Expression (physiology)
• Genes, fos (physiology)
• In Situ Hybridization
• Lactates (metabolism)
• Nicardipine (therapeutic use)
• Oligonucleotide Probes
• Pyrithiamine (antagonists & inhibitors, toxicity)
• Rats
• Rats, Sprague-Dawley
• Wernicke Encephalopathy (chemically induced, metabolism, pathology)