Journal of Okayama Medical Association
Published by Okayama Medical Association

<Availability>
Full-text articles are available 3 years after publication.

Methylguanidineの発作発現機構に関する生理学的研究

Shimizu, Yoshihisa
Thumnail 102_405.pdf 855 KB
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.
Keywords
methylguanidine
guanidino compound
experimental seizures
GABA-receptor antagonist
anticonvulsant
ISSN
0030-1558
NCID
AN00032489