[The genetic characteristics of the brain alpha 2-adrenergic and S2-serotoninergic systems in the realization of the tail-jerk pain reflex and its morphine suppression in rats].

Experiments were conducted on two inbred rat strains--WAG/G and Fischer-344. The WAG/G rats were found to increase the density of brain cortical mu-opiate and alpha 2-adrenergic receptors, short latency of tail immersion from hot water, decreased analgesic action of 5 mg/kg of intraperitoneal morphine and pronounced analgesic action of 10 micrograms of intracerebral ventricular clonidine The Fischer-344 rats increased S2-receptor affinity, protracted pain latency, increased the analgesic action of morphine (5 mg/kg i.p.), serotonin (0.5 microgram i.c.v.), and ketanserine (1 microgram i.c.v.). The intracerebral ventricular administration of clonidine, serotonin, yohimbine, and ketaserine significantly increased the analgesic action of morphine in the two strains. It is suggested that a prompt pain response and increased analgesic action of morphine in Fischer-344 rats may be determined by higher affinity of serotoninergic receptors, but a slow pain reflex and decreased morphine-induced analgesia of WAG/G rats may be caused by the high density of brain cortex alpha 2-adrenergic receptors.