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Objective To investigate the effects of antisense glutamic acid decarboxylase (GAD_ 67 ) oligodeoxynucleo- tide (ODN) on behavior, seizure threshold and EEG of hippo campus in the epileptic rats induced by pentylenetetrazol (PTZ). Methods A model of chronic epilepsy in rats was established by PTZ. The inhibit ion of GAD_ 67 mRNA expression in hippocampus was selectively induced by ant isense oligodeoxynucleotide of GAD_ 67 . The effect of antisense GAD_ 67 ODN o n behavior, seizure threshold and EEG recording of kindled rats was examined. Results Antisense GAD_ 67 ODN could inhibit the expression of GAD_ 67 mRNA and t h e concentration of GABA. It also could significantly shorten the latencies of s e izure and increase the level of seizure and the frequency of epileptiform discha rges. Conclusion The gene of GAD_ 67 may be an anti-seizure gene, which might in hibit epileptiform discharge. The treatment of epilepsy by GAD_ 67 gene wi ll have a bright future.
Objective To investigate the effects of antisense glutamic acid decarboxylase (GAD_67) oligodeoxynucleotid (ODN) on behavior, seizure threshold and EEG of hippo campus in the epileptic rats induced by pentylenetetrazol (PTZ). Methods A model of chronic epilepsy in rats was established by PTZ. The inhibit ion 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. Results Antisense 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 dischages. Conclusion The gene of GAD_67 may be anti- seizure gene, which might in hibit epileptiform discharge. The treatment of epilepsy by GAD_67 gene wi ll have a bright future.