Seizure-induced damage in the substantia nigra pars reticulata: lesions in the frontal cortex prior to the seizure period mitigate the damage.
Flurothyl-induced status epilepticus in the rat causes a hypermetabolic necrosis in the substantia nigra pars reticulata (SNPR). We studied if cortically generated excitatory input into the SNPR was causative of the structural damage. Rats were subjected to a unilateral frontal cortex lesion prior to induction of 40 min status epilepticus. A distinct mitigation in the size of the necrotic region in the ipsilateral SMPR was noted when compared to the contralateral side of the same animals (N = 10). No side difference was noted in animals where a lesion of similar size was placed in the parietal cortex region (N = 2) or in unlesioned animals subjected to seizures (N = 4). Neither analyses of energy metabolites in the cerebral cortex nor EEG revealed any side differences during seizures in the animals with lesions in the frontal cortex. This suggests that difference in seizure intensity was not the explanation for the mitigation of SNPR damage. It is suggested that the excitatory input from the frontal cortex was necessary for development of neuronal necrosis in the SNPR due to seizures.
Ingvar
M
M
Department of Histology and Neurobiology, Karolinska Institute, Stockholm, Sweden.
D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D004734:Energy Metabolism; D005481:Flurothyl; D005625:Frontal Lobe / Q000378:metabolism / Q000502:physiology*; D008297:Male; D009336:Necrosis; D051381:Rats; D011919:Rats, Inbred Strains; D012640:Seizures / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology; D013378:Substantia Nigra / Q000378:metabolism / Q000473:pathology*
D000596:Amino Acids; D005481:Flurothyl