Congenital brain dysplasias of different genesis can differently affect susceptibility to pilocarpine- or kainic acid-induced seizures in the rat.
Interruption of neurogenesis and/or neuronal migration produces brain dysplasia modifying susceptibility to epileptic seizures in adulthood. The course of neurogenesis has a strictly defined time-table. Consequently, the developmental stage at which the interruption occurs determines what functional subsystem potentially involved in epileptogenesis will suffer from irreversible neuronal deficit. The present study attempts to verify a hypothesis that brain dysplasias of different genesis should also lead to different susceptibility to seizures evoked by receptor agonists of different functional specificity, like kainic acid or pilocarpine, a cholinergic or glutaminergic agonist, respectively. Pregnant Wistar rats were exposed to gamma-rays on gestation days 13, 15, 17 or 19 (E13, E15, E17 or E19). Sixty-day-old offsprings of the females were injected with kainic acid or pilocarpine to evoke status epilepticus. During a 6-h period following the injection, motor manifestations of seizure activity were recorded. Generally, the intensity of pilocarpine-induced symptoms was relatively low in rats irradiated on E13 or E15 but high in rats irradiated on E17 or E19. In rats treated with kainic acid, the trend was opposite, viz. the later the prenatal irradiation was performed, the less intense epileptic symptoms were induced in adulthood. The data provide evidence that dysplasias acquired during prenatal development may significantly amplify or reduce the brain susceptibility to seizures. However, this relation depends not only on the developmental stage at which the dysplasias were produced but also on the functional specificity of epileptogenic stimuli used in the experimental model of epilepsy.
Setkowicz
Zuzanna
Z
Department of Neuroanatomy, Institute of Zoology, Jagiellonian University, 6 Ingardena St, 30 060 Kraków, Poland.
Janicka
Dominika
D
Kowalczyk
Anna
A
Turlej
Anna
A
Janeczko
Krzysztof
K
D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D001927:Brain Diseases / Q000151:congenital* / Q000209:etiology / Q000473:pathology*; D003292:Convulsants; D004305:Dose-Response Relationship, Drug; D004569:Electroencephalography / Q000187:drug effects; D005260:Female; D005720:Gamma Rays; D007608:Kainic Acid / Q000008:administration & dosage / Q000494:pharmacology*; D010862:Pilocarpine / Q000008:administration & dosage / Q000494:pharmacology*; D011247:Pregnancy; D011833:Radiation Injuries, Experimental / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D012640:Seizures / Q000139:chemically induced*; D013226:Status Epilepticus / Q000503:physiopathology
D003292:Convulsants; D010862:Pilocarpine; D007608:Kainic Acid