Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

The present study was undertaken to clarify the role of histaminergic neuron system on amygdaloid kindled seizures in rats. A significant decrease in histamine contents in the amygdala was observed after development of amygdaloid kindling. Histidine inhibited amygdaloid kindled seizures at doses causing an increase in histamine contents of the brain. H1-antagonists (diphenhydramine and chlorpheniramine) attenuated histidine-induced inhibition of amygdaloid kindled seizures, however no significant antagonism was observed with H2-antagonists (zolantidine and ranitidine). The development of amygdaloid kindling was retarded by repeated administration of histidine. Both intracerebroventricular (i.c.v.) and intraperitoneal (i.p.) injections of H3-antagonists, thioperamide and clobenpropit, resulted in a dose-related inhibition of amygdaloid kindled seizures. An inhibition induced by thioperamide was antagonized by an H3-antagonist [(R)-alpha-methylhistamine] and H1-antagonists (diphenhydramine and chlorpheniramine). On the other hand, H2-antagonists (zolantidine and ranitidine) caused no antagonistic effects. Metoprine, an inhibitor of N-methyltransferase was also effective in inhibiting amygdaloid kindled seizures, and this effects was augmented by thioperamide treatment. These findings suggest that histaminergic mechanisms play a suppressive role in amygdaloid kindled seizures through histamine H1-receptors.

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Presentation Number SAkamei0281
Keywords: Amygdala, Kindled seizures, Histamine, Histidine, H3-antagonists