INVOLVEMENT OF INTRATHALAMIC GABA(B) NEUROTRANSMISSION IN THE CONTROL OF ABSENCE SEIZURES IN THE RAT

The role of intrathalamic GABA(B) neurotransmission in the control of absence seizures was investigated. In rats with genetic absence epilepsy, bilateral injections of R-baclofen (50, 100 and 200 ng/side), a selective GABA(B) receptor agonist, into the specific relay nuclei and the reticular nuclei of the thalamus increased spontaneous spike and wave discharges in a dose-dependent fashion, whereas injections of a GABA(B) antagonist CGP 35 348 (1, 2.5 and 5-mu-g/side) into the same sites decreased these seizures dose-dependently. The effect of R-baclofen (200 ng/side) on spike and wave discharges could be blocked by a subsequent injection of CGP 35 348 (1-mu-g/side) at the same site. Injections of R-baclofen (200 ng) or CGP 35 348 (5-mu-g) into the midline thalamus had no effect on these seizures. In non-epileptic rats, bilateral injections of R-baclofen (1-mu-g/side) into the specific relay nuclei induced synchronized rhythmic oscillations on the cortical electroencephalogram. The results suggest that GABA(B) receptors in the ventrolateral thalamus and in the reticular nuclei are involved in an oscillatory activity which underlies the rhythmic spike and wave discharges recorded during spontaneous generalized non-convulsive seizures.