| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Research Abstract |
0pioids are known to inhibit the nerve transmission at the somatic sensory area of the cerebral cortex and sensory nerve area of the trigeminal nerve. However, there was no report about what kind of neurotransmitter or neurotransmitters are involved in this transmission. The effects morphine and related several mu opioids were determined on the output of preloaded tritium noradrenaline (NA), acetylcholine (Ach) and serotonin (5-HT) from the synaptosomes caused by high concentration of potassium and field stimulation from whole area of the cerebral cortex, from somatic sensory area of the cerebral cortex and sensory area of the trigeminal nerve. Pretreatment with morphine (10^<-3>-10^<-5>M), DAGO (5x10^<-3> -5x210^<-4>M), morphiception (5x10^<-3> -5x10^<-4>M), beta-endorphin (5x10^<-4>M) and methionine-enkephaline (5x10^<-4>) significantly inhibited the output of NA,Ach and 5-HT caused by high potassium and field stimulation. These inhibitory output of all neurotransmitters tested were
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suppressed by pretreatment with mu receptor antagonists, naloxone (10^<-3>-5x10^<-5>M) and beta-funaltrexamine (5x10^<-3>-5x10^<-4>M). However, these suppressing effects of kappa receptor antagonists, pentazocine (>5x10^<-3>M) and premazocin (>5x10^<-3>M) were appeared to be weaker than the mu antagonists. Next, we studied the effects of subtypes of opioids on the synaptosomal (Na^++K^+) -ATPase activity from whole area of the cerebral cortex to investigate the mechanisms of inhibitory action of depolarization by the opioids in the presence of several heavy metalions. Mu agonists, morphine and morphiceptin and dynorphin a 3-8 but not the kappa agonist dynorphin- (1-8) -octapeptide, stimulated the (Na^++K^+) -ATPase suppressed by Fe^<2+>.
These results suggest that mu opioid agonists may involve the neurotransmission in the somatic sensory area of the cerebral cortex or sensory nerve area of the trigeminal nerve and may stimulate the suppressed (Na^++K^+) -ATPase activity by interacting with Fe^<2+> at mu opioid receptor site, and may finally inhibit the deporalizing action presynaptically at this area. Less
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