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Abstract
Excitatory am ino acids have been implicated in the seizures and seizure-related brain damage (SRBD) resulting from soman intoxication. Memantine (Mem) is an open channel blocker of the glutaminergic NMDA receptor subtype reported to have anticonvulsant activity against soman. The aim of the present experiments was to evaluate the effect of Mem on electrographic seizure activity (EGSA) and SRBD produced by soman. Male rats were implanted with cortical screw electrodes for recording bipolar electrocorticogram s and allowed to recover for 5-7 days. EGSA was precipitated by injecting soman (180 mug/ kg, SC) 30 m in after HI6 (125 mg/ kg, IP) pretreatm ent. Saline, Mem (18 mg/ kg), atropine (A;10 mg/ kg), or Mem + A was adm inistered IP either 5 or 40 m in after the onset of EGSA. Saline-treated anim als displayed limbic convulsive behaviors and EGSA lasting for 4 or m ore hours. Mem or Mem + A suppressed behavioral signs of soman intoxication, but did not terminate EGSA or prevent SRBD. These results indicate that soman-induced seizures are not ameliorated by Mem or Mem + A, and that the presence or absence of som an-induced seizures cannot be verified reliably through behavioral observations alone.