Proto-oncogene c-fos induction in thiamine-deficient encephalopathy. Protective effects of nicardipine on pyrithiamine-induced lesions.
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.
Munujos
P
P
Departament de Bioquímica i Biologia Molecular, Universitat Autonoma de Barcelona, Spain.
Vendrell
M
M
Ferrer
I
I
D000818:Animals; D005260:Female; D015870:Gene Expression / Q000502:physiology*; D016762:Genes, fos / Q000502:physiology*; D017403:In Situ Hybridization; D007773:Lactates / Q000378:metabolism; D009529:Nicardipine / Q000627:therapeutic use*; D015345:Oligonucleotide Probes; D011745:Pyrithiamine / Q000037:antagonists & inhibitors* / Q000633:toxicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D014899:Wernicke Encephalopathy / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*
D007773:Lactates; D015345:Oligonucleotide Probes; D011745:Pyrithiamine; D009529:Nicardipine