The alteration of γ-aminobutyric acid-transaminase expression in the gerbil hippocampus induced by seizure

被引:36
作者
Kang, TC
Park, SK
Bahn, JH
Jeong, SG
Jo, SM
Cho, SW
Choi, SY
Won, MH [1 ]
机构
[1] Hallym Univ, Coll Med, Dept Anat, Chunchon 200702, South Korea
[2] Hallym Univ, Coll Life Sci, Dept Genet Engn, Chunchon 200702, South Korea
[3] Univ Ulsan, Coll Med, Dept Biochem, Seoul 138736, South Korea
关键词
epilepsy; GABA metabolism; GABA transaminase; gerbil; hippocampus; immunohistochemistry;
D O I
10.1016/S0197-0186(01)00002-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
It is well established that GABA degradation may play a key role in epileptogenesis. However, whether or not the expression of GABA-transaminase (GABA-T), which catalyzes GABA degradation and participates in the neuronal metabolism via GABA shunt, changes chronologically after on-set of seizure remains to be clarified. To identify the change of GABA-T expression in seizure, GABA-T expression in the gerbil hippocampus, associated with different sequelae of spontaneous seizures, was investigated. The distribution pattern of GABA-T immunoreactive neurons in the hippocampus between the seizure-resistant and pre-seizure group of seizure sensitive gerbils was similar. Interestingly, at 30 min postictal, the enhancement of GABA-T immunoreactivity in the perikarya was apparently observed. This contrasted with the decline in GABA-T immunoreactivity in the granular and pyramidal layer. At 12-24 h postictal, GABA-T immunoreactivity in the hilar neurons had declined significantly. However, the GABA-T immunoreactivity in the granular layer increased. These findings suggest that in the gerbil, the alteration in GABA-T expressions may play an important role in the self-recovery mechanism from seizure attack via both GABA degradation and regulation of neuronal metabolism. (C) 2001 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:609 / 614
页数:6
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