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Vulnerable seizure activity in neonatal brain through little COX activity

Chung, Jee-In; Kim, A Young; Jang, You Na; Baura, Sumit; Kim, So-Yeon; Baik, Eun Joo
Department of Physiology, Ajou University School of Medicine; Chronic Inflammatory Disease Research Center, Ajou Research Institute for Innovative Medicine
BACKGROUND: Seizures occurs with abnormal excessive electrical activity in the brain. The seizure activity is more common in young children than adults. Most neonatal seizures are extremely difficult to control with current anti-epileptic drugs (AEDs). In the previous our reports, COX-2 inhibitors aggravate KA-induced seizures and PGF2 might act as endogenous anticonvulsant in the adult mice. Therefore, we assumed whether management of COX activity regulates KA-induced neonatal seizure.
OBSERVATIONS: Neonatal (post-natal day 9) mice are far more prone to KA-induced seizures than the adult (P35). The seizure activities in the adult, which was aggravated by COX inhibition, showed less than those in the neonate. However, the neonate seizure activities were not affected by COX inhibition. Interestingly, in the brain, COXs mRNA and protein expression increased during development. The maturation of COXs activity was correlated with glycosylation. However, in the neonate brain COX-1/2 were rarely expressed and could not be activated by excitable stimulus. By western blot analysis, sqRT-PCR and EIA assay, the neonate hippocampus expressed little COX-1/2 and little PGF2with/without KA stimulation, whilst the adult hippocampus responded the increased COX-2 and PGF2by KA. Also, the seizure activity in the neonate was alleviated by intracisternal PGF2 administration.
CONCLUSIONS: In the present study, the expression and activity of COXs were developed and activated with brain maturation during development. Our findings suggested that neonatal vulnerability to seizure is closely associated with little COXs activity and following little PGF2release.
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