Febrile Seizure-induced Neuroexcitability in Immature Rat Hipocampus.
- Author:
Bong Keun CHOI
1
;
Kyu Geun HWANG
;
Hae Rahn BAE
Author Information
1. Department of Pediatrics, Dong-A University Medical School, Busan, Korea. kghyang@daunet.donga.ac.kr
- Publication Type:Original Article
- Keywords:
Seizure;
Febrile;
Rat;
Synaptic transmission;
Receptor;
AMPA
- MeSH:
Rats;
Animals
- From:Korean Journal of Pediatrics
2004;47(9):992-1001
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: To determine whether febrile seizure enhances neuroexcitability by altering synaptic transmission and whether febrile seizure-induced hyperexcitability leads to long-lasting neuronal death. METHODS: We investigated the expression of synaptic and postsynaptic proteins and the apoptosis of neuronal cells in rat pup hippocampus after hyperthermic seizure using immunoblotting and confocal microscopy. RESULTS: Hyperthermic seizure enhanced the long-term expressions of presynaptic proteins such as syntaxin, VAMP, SNAP-25 and nSec1, whereas that of NSF was decreased. The expressions of postsynaptic NMDA receptors 1, 2a and 2b were up-regulated. The expression of postsynaptic AMPA glutamate receptors 1 month after hyperthermic seizures altered by way of increasing the ratio of GluR1 to GluR2 and decreasing NSF-GluR2 interaction, which leads to the formation of Ca2+permeable AMPA receptors and enhanced toxicity. However, in spite of enhanced neuroexcitability, there was a transient increase of neuronal death in hipocampus one week after hyperthermic seizure, but returned to baseline one month later. CONCLUSION: These results demonstrate both presynaptic and postsynaptic forms of long-term enhancement of glutamate synaptic transmission after hyperthermic seizure and support the idea that early-life febrile seizure might have persistent effects on neuronal excitability in the hippocampus.
