Kamei C, Ishizawa K, Kakinoki H, Fukunaga M
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Okayama University, Japan.
Epilepsy Res. 1998 May;30(3):187-94. doi: 10.1016/s0920-1211(98)00005-9.
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 and metoprine 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. These findings suggest that histaminergic mechanisms play a suppressive role in amygdaloid kindled seizures through histamine H1-receptors.
