Karadag, CHUlugol, ADokmeci, DDokmeci, I2024-06-122024-06-1219960021-5198https://doi.org/10.1254/jjp.71.109https://hdl.handle.net/20.500.14551/22540Morphine is known to release histamine from mast cells. It is also known that histamine receptors mediate some of morphine's effects on the central nervous system. The contribution of H-1- and H-2-receptors to the effect of morphine on maximal electroconvulsive shock in mice was investigated in the present experiments. Morphine showed a dose-dependent anticonvulsive effect, but produced spontaneous clonic convulsions at higher doses (100 mg/kg, i.p.). The anticonvulsive effect of morphine (1 mg/kg, i.p.) was antagonized by histamine Hi-receptor antagonists, dimethindene (0.1 mg/kg, i.p.), promethazine (0.4 mg/kg, i.p.) and pheniramine (30 mg/kg, i.p.), and naloxone (10 mg/kg, i.p.), but not by the H-2-receptor antagonist ranitidine (10-50 mu g, i.c.v.). These results show that morphine has an anticonvulsive effect via histamine H-1-receptors against maximal electroconvulsive shock in mice.en10.1254/jjp.71.109info:eu-repo/semantics/openAccessMorphineAnticonvulsive EffectHistamineHistamine H-1-ReceptorMaximal Electroconvulsive ShockCentral Nervous-SystemMast-CellsBrain HistamineMouse-BrainRatTransmitterInvolvementReceptorsTurnoverReleaseArticle712109112N/AWOS:A1996UT290000032-s2.0-00296617338835636N/A