Effects of antisense glutamic acid decarboxylase oligodeoxynucleotide on epileptic rats induced by pentylenetetrazol.
- Author:
Xiaohua HE
1
;
Wei WANG
;
Xuzhong RUAN
;
Wenxin LI
;
Liang ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Electroencephalography; Epilepsy; chemically induced; physiopathology; Glutamate Decarboxylase; genetics; pharmacology; Hippocampus; physiopathology; Isoenzymes; genetics; pharmacology; Kindling, Neurologic; Male; Oligonucleotides, Antisense; pharmacology; Pentylenetetrazole; Rats; gamma-Aminobutyric Acid; analysis
- From: Chinese Medical Journal 2002;115(3):425-429
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the effects of antisense glutamic acid decarboxylase (GAD(67)) oligodeoxynucleo-tide (ODN) on behavior, seizure threshold and EEG of hippocampus in the epileptic rats induced by pentylenetetrazol (PTZ).
METHODSA model of chronic epilepsy in rats was established by PTZ. The inhibition of GAD(67) mRNA expression in hippocampus was selectively induced by antisense oligodeoxynucleotide of GAD(67). The effect of antisense GAD(67) ODN on behavior, seizure threshold and EEG recording of kindled rats was examined.
RESULTSAntisense GAD(67) ODN could inhibit the expression of GAD(67) mRNA and the concentration of GABA. It also could significantly shorten the latencies of seizure and increase the level of seizure and the frequency of epileptiform discharges.
CONCLUSIONThe gene of GAD(67) may be an anti-seizure gene, which might inhibit epileptiform discharge. The treatment of epilepsy by GAD(67) gene will have a bright future.
