Effects of zonisamide (AD-810) on tungstic acid gel-induced thalamic generalized seizures and conjugated estrogen-induced cortical spike-wave discharges in cats.
Effects of zonisamide (AD-810, CI-912) were examined on tungstic acid gel-induced thalamic generalized seizures and conjugated estrogen-induced cortical spike-wave discharges in gallamine-immobilized cats. Zonisamide prolonged the interictal periods of the generalized seizures by thalamic (centralis lateralis) application of tungstic acid gel (50 microliters) and, at the higher doses, abolished the seizures; its potency was near that of phenobarbital. Zonisamide abolished the spike-wave discharges by cortical (posterior lateralis) application of 2% conjugated estrogens (CE); its potency was stronger than that of dipropylacetate or trimethadione, but slightly less than that of phenytoin, phenobarbital, or carbamazepine. Zonisamide did not affect the posttetanic potentiation of the monosynaptic reflexes (ventral root potentials) in urethane-chloralose-anesthetized spinal rats. From these results, it is suggested that zonisamide suppresses both seizures originating from the thalamus and the cortex through the mechanism differing from that of phenytoin. Zonisamide appears to be effective in primary generalized seizures, especially the grand mal epilepsies, in addition to being effective in cortical epilepsies.
D000818:Animals; D002415:Cats; D002540:Cerebral Cortex / Q000187:drug effects*; D004967:Estrogens; D005260:Female; D007555:Isoxazoles / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D010080:Oxazoles / Q000494:pharmacology*; D012640:Seizures / Q000139:chemically induced / Q000188:drug therapy*; D013788:Thalamus / Q000187:drug effects*; D014414:Tungsten; D017973:Tungsten Compounds; D000078305:Zonisamide
D004967:Estrogens; D007555:Isoxazoles; D010080:Oxazoles; D017973:Tungsten Compounds; D000078305:Zonisamide; C021101:tungstic(VI) acid; D014414:Tungsten