T. Halonen et al., ALPHA(2)-ADRENOCEPTOR AGONIST, DEXMEDETOMIDINE, PROTECTS AGAINST KAINIC ACID-INDUCED CONVULSIONS AND NEURONAL DAMAGE, Brain research, 693(1-2), 1995, pp. 217-224
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.