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A physiological study of methylguanidine-induced seizures

Authors
Publisher
岡山医学会
Publication Date
Keywords
  • Methylguanidine
  • Guanidino Compound
  • Experimental Seizures
  • Gaba-Receptor Antagonist
  • Anticonvulsant

Abstract

The CNS action of methylguanidine (MGua) was investigated in male S. D. rats. The effects of a GABA-agonist and anticonvulsants on the MGua-induced EEG changes were studied. Several min after an intraventricular injection of 10 μl of a MGua solution (100 mM), rats displayed running fits, tonic- and clonic-convulsion with myoclonic twitching accompanied by polyspikes and spike bursts in the EEG. Diazepam (DZP) (10mg/kg, i. p.) inhibited the convulsive activity, but ethosuximide (ESM) (200mg/kg, i. p.) showed no effect. Sporadic spike discharges began 2-10 min after MGua (1 μmol) application to the pia mater of the sensorimotor cortex, and thereafter, a recurrent ictal seizure pattern (ISP) was induced. The ISPs were suppressed by DZP (10mg/kg) and phenobarbital (PB) (20mg/kg), injected after the completion of ISPs induced by MGua. Spike discharges were not induced by the application of MGua together with muscimol (50nmol), although muscimol did not suppress the ISPs following their completion. Intraperitoneal injection of either ESM (50-200mg/kg), valproate (200mg/kg) or phenytoin (25 mg/kg), after the completion of ISPs, did not affect the ISPs. These findings suggest that GABAA receptors might participate in the induction mechanism of MGua-induced seizure activities, and that DZP and PB receptors might a play role in the mechanism which suppresses MGua-induced Seizures.

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