Long-term prenatal stress increases susceptibility of N-methyl-D-aspartic acid-induced spasms in infant rats.
10.3345/kjp.2018.61.5.150
- Author:
Hyeok Hee KWON
1
;
Taekwan LEE
;
Jinpyo HONG
;
Dong Woon KIM
;
Joon Won KANG
Author Information
1. Department of Medical Science, College of Medicine, Chungnam National University, Daejeon, Korea. childlove@cnu.ac.kr
- Publication Type:Original Article
- Keywords:
Infantile spasms;
Prenatal exposure delayed effects;
Potassium-chloride symporters;
Glutamate decarboxylase;
Gamma-Aminobutyric acid
- MeSH:
Animals;
Epilepsy;
gamma-Aminobutyric Acid;
Glutamate Decarboxylase;
Humans;
Immobilization;
Immunohistochemistry;
Infant*;
Infant, Newborn;
N-Methylaspartate;
Prenatal Exposure Delayed Effects;
Rats*;
Seizures;
Spasm*;
Spasms, Infantile
- From:Korean Journal of Pediatrics
2018;61(5):150-155
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Infantile spasms, also known as West syndrome, is an age-specific epileptic seizure. Most patients with this condition also exhibit delayed development. This study aimed to determine the effect of long-term prenatal stress on susceptibility to infantile spasms. METHODS: We subjected pregnant rats to acute or chronic immobilization stress. Resulting offspring received N-methyl-D-aspartic acid (15 mg/kg, intraperitoneally) on postnatal day 15, and their behaviors were observed 75 minutes after injection. The expression of KCC2 and GAD67 was also determined using immunohistochemistry. RESULTS: Exposure to long-term prenatal stress increased the frequency of spasms and decreased the latency to onset of spasms compared with offspring exposed to short-term prenatal stress. Expression of KCC2 and GAD67 also decreased in the group exposed to long-term prenatal stress compared with the group exposed to short-term prenatal stress. CONCLUSION: Our study suggests that exposure to long-term prenatal stress results in increased susceptibility to seizures.
