SEIZURE ACTIVITY RESULTS IN A RAPID INDUCTION OF NUCLEAR FACTOR-KAPPA-B IN ADULT BUT NOT JUVENILE RAT LIMBIC STRUCTURES

Authors
Citation
Yq. Rong et M. Baudry, SEIZURE ACTIVITY RESULTS IN A RAPID INDUCTION OF NUCLEAR FACTOR-KAPPA-B IN ADULT BUT NOT JUVENILE RAT LIMBIC STRUCTURES, Journal of neurochemistry, 67(2), 1996, pp. 662-668
Citations number
44
Categorie Soggetti
Biology,Neurosciences
Journal title
ISSN journal
00223042
Volume
67
Issue
2
Year of publication
1996
Pages
662 - 668
Database
ISI
SICI code
0022-3042(1996)67:2<662:SARIAR>2.0.ZU;2-T
Abstract
Previous studies have indicated that increased formation of oxygen fre e radicals is likely to participate in the cascade of events leading t o neuronal damage following kainic acid (KA)-induced seizure activity. As reactive oxygen species are involved in signal transduction pathwa ys leading to nuclear factor-kappa B (NF-kappa B) activation, we exami ned the effects of KA treatment on the activation of NF-kappa B in adu lt and juvenile rat brain. For comparison, changes in two other transc ription factors, activator protein-1 (AP-1) and Spl, were also determi ned. In adult rat piriform cortex and hippocampus, significant inducti on of NF-kappa B was observed at 4 h after KA injection, and the maxim al increase was reached at 8-16 h posttreatment. NF-kappa B binding ac tivities returned to control levels by 5 days after injection. NF-kapp a B binding activities were slightly decreased in adult rat cerebellum at 8 and 16 h after KA treatment. In the juvenile rat, no significant changes in NF-kappa B binding activity were observed in piriform cort ex, hippocampus, and cerebellum after KA injection. Changes in AP-1 bi nding activity were qualitatively similar to those observed with NF-ka ppa B in adult but not juvenile rat brain, as AP-1 was significantly i nduced in juvenile piriform cortex and hippocampus following KA inject ion. On the other hand, little or no changes in Sp1 activity were dete cted in adult and juvenile rat brain. Our results provide further evid ence that oxidative stress participates in neuronal damage resulting f rom KA-induced seizure activity.