ALPHA(2)-ADRENOCEPTOR AGONIST, DEXMEDETOMIDINE, PROTECTS AGAINST KAINIC ACID-INDUCED CONVULSIONS AND NEURONAL DAMAGE

Kainic acid (KA)-induced convulsions are accompanied by histopathologi cal changes that are most prominent in the temporal lobe structures. I n the present study, we investigated whether a selective alpha(2)-adre noceptor agonist, dexmedetomidine could attenuate KA-induced epileptic convulsions and subsequent neuronal damage in the rat hippocampus. Ra ts were pretreated 30 min before KA injection (9 mg/kg, i.p.) with dex medetomidine (3 mu g/kg, s.c.). The behavior of animals was observed f or at least 3 h. Dexmedetomidine suppressed the development (p < 0.001 ), generalization (p < 0.05) and severity (p < 0.01) of convulsions. I n addition, histological analysis revealed that dexmedetomidine-treate d animals without convulsions or with only partial convulsions had no neuronal damage in the principal cell layers of the hippocampus. A sel ective alpha-antagonist, atipamezole (1 mg/kg, s.c.) potentiated KA-in duced convulsions and increased the mortality in status epilepticus. I n conclusion, the present study demonstrated that dexmedetomidine, in addition to possessing anticonvulsant properties, has a neuroprotectiv e effect in the KA model of status epilepticus.