Open AccessThe Role of Histamine H1-Receptors in the Anticonvulsive Effect of Morphine against Maximal Electroconvulsive Shock in Mice
Author(s) -
Çetin Hakan Karadağ,
Ahmet Ulugöl,
Dikmen Dökmeci,
İsmet Dökmeci
Publication year - 1996
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.71.109
Subject(s) - electroconvulsive shock , morphine , histamine , histamine h1 receptor , anesthesia , pharmacology , shock (circulatory) , chemistry , medicine , receptor , antagonist
Morphine 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 H1- and H2-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 H1-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 H2-receptor antagonist ranitidine (10-50 micrograms, i.c.v.). These results show that morphine has an anticonvulsive effect via histamine H1-receptors against maximal electroconvulsive shock in mice.