Febrile Seizure-induced Neuroexcitability in Immature Rat Hipocampus |
Bong Keun Choi1, Kyu Geun Hwang2, Hae Rahn Bae1 |
1Department of Pediatrics, Dong-A University Medical School, Busan, Korea 2Department of Physiology, Dong-A University Medical School, Busan, Korea |
미성숙 흰쥐 해마에서 열성경련에 의한 신경흥분성의 증가 |
최봉근1, 배혜란2, 황규근1 |
1동아대학교 의과대학 소아과학교실 2동아대학교 의과대학 생리학교실 |
Correspondence:
Kyu Geun Hwang, Email: kghyang@daunet.donga.ac.kr |
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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. |
Key Words:
Seizure, Febrile, Rat, Synaptic transmission, Receptor, AMPA |
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