Sequential Change of Nitric Oxide Synthase in Rat Hippocampus after Kanic Acid-induced Seizure.
- Author:
Jong Kwon PARK
1
;
Chan PARK
;
Min Jeong KANG
;
Kyoung Lan KANG
;
Jae Ryong LEE
;
Jung Hye KIM
;
Jin Hwa YOO
;
Young Buhm HUH
;
Hee Kyoung AHN
Author Information
1. Department of Anatomy, College of Medicine, Kyung Hee University, Korea.
- Publication Type:Original Article
- Keywords:
NADPH-diaphorase;
Neuronal nitric oxide synthase;
Kainic acid;
Hippocampus
- MeSH:
Animals;
Brain;
Dentate Gyrus;
Hippocampus*;
Kainic Acid;
Neurons;
Nitric Oxide Synthase Type I;
Nitric Oxide Synthase*;
Nitric Oxide*;
Rats*;
RNA, Messenger;
Seizures*;
Silver
- From:Korean Journal of Anatomy
2000;33(5):511-518
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
We have investigated the neural cell damage and the change in the expression of NOS in the rat hippocampus, one of the brain structures most vulnerable to seizures. Rats were injected with kainic acid (KA) and sacrificed 6 h, 1 d, 3 d and 6 d after KA administration. The neural cell damage and the expression pattern of NOS was studied using silver impregnation, NADPH-diaphorase (NADPH-d) histochemistry and reverse transcription-polymerase chain reaction (RT-PCR) analysis. Silver impregnation revealed that kainic acid caused pyramical cell damage which was most severe in the CA1/CA2 subfield and hilus and to a lesser degree in the CA3 region. The optical densities of NADPH-d-positive neurons in the CA1, CA3 and dentate gyrus (DG) regions of the hippocampus were shown to have increased in samples obtained 1 d and 3 d after injection of KA. The number of NADPH-d-positive neurons in the CA1 and CA3 regions of the hippocampus was shown to have decreased in samples obtained 3 d and 6 d after injection of KA. However, the number of NADPH-d-positive neurons in the DG region did not change significantly. The increase in the levels of nNOS, iNOS and eNOS mRNA reached maximal values in samples obtained 1 d after KA treatment. Our findings indicate that the KA-induced seizures induce neural cell damage, increase NOS activity and upregulate the expression of NOS mRNA, which suggests the possibility of a functional role of NOS in bringing about changes in the cells in the hippocampus following seizures.
