| Apoptosis, P53, bax and Bcl-2 Protein Expressions in Neonatal rat Hippocampus by Kainic Acid-induced Seizure |
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Shin Weon Yun, Soo Ahn Chae, Eung sang Choi, Byoung Hoon Yoo |
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Department of P ediatrics, College of M edicine, Chung-Ang University, Seoul, Korea |
| 신생 쥐 해마에서 Kainic Acid 유발 경련으로 인한 세포자멸사(apoptosis)와 P53, Bax, Bcl-2 단백 발현에 관한 연구 |
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윤신원, 채수안, 최응상, 유병훈 |
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중앙대학교 의과대학 소아과학교실 |
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| Abstract |
Purpose
: Apoptosis is a process of active cell death which has been suggested to be part of
hippocampal cell loss caused by kainic acid(KA). Immature rats showed higher susceptibility and
mortality to KA but did not develop recurrent seizure, long term behavioral or neuropathologic
changes. We investigated whether this was due to age-dependent resistance, and elucidated the
molecular mechanics which mediate P53-induced apoptosis, identifying bax and bcl-2 as P53
protein expressions that serve as a paradigm on how the balance of bcl-2 to bax is differentially
altered by apoptotic stimuli.
Methods
: Sprague-Dawley rats were classified into postnatal age(P) 10, 15, 20 and 30 days and
given specific doses of i.p. KA(P10; 3mg/kg, P15; 4mg/kg, P20; 8mg/kg, P30; 10mg/kg). Only rats
that achieved continuous clonic seizure were selected and decapitated at 24, 48, and 72h(n=15 each
age). We analysed P53, bax and bcl-2 protein expressions by immunohistochemistry as well as
apoptosis by TUNEL in each group.
Results
: KA-induced hippocampal cell death first appeared in P20. Remarkable expressions of
apoptosis, P53 and bax, while bcl-2 proteins were suppressed were observed at 48 hours
following KA in P20 and the most prominently affected areas were hippocampal CA1 and CA3
neurons. Similar results were obtained in P30.
Conclusion
: Induction of P53, a growth regulatory gene which has been implicated in apoptosis
and the changes in bcl-2 to bax ratio may be important to KA mediated excitotoxicity of specific
regions during the critical period of developing rat brain. |
| Key Words:
Kainic acid(KA), Hippocampus, Immature rat, Apoptosis, P53, Bax, Bcl-2 protein |
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