モルヒネ耐性の形成で区分される針鎮痛発現系と鎮痛抑制系で抑制されている鎮痛発現系

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In our previous report, it was supposed that intrinsic mechanism producing morphine tolerance might be existed in acupuncture analgesia inhibitory system since abolished acupuncture and morphine analgesia after treatment of enough doses of morphine to develop morphine tolerance reappeared by lesion of the lateral centromedian nucleus of thalamus (1-CM) which had been identified as acupuncture inhibitory system and since after lesion of the 1-CM, morphine tolerance was hardly to develop. However, it was found in our recent experiment that 1) two afferent pathways to respond to acupuncture stimulation were recognized in the central nervous system : One is the pathway from acupuncture point to the hypophysis (R2) which is the pathway to produce acupuncture analgesia and the other is the pathway (R1) completely inhibited by acupuncture inhibitory system such as the 1-CM during acupuncture analgesia and 2) acupuncture analgesia produced by R2 was completely antagonized by naloxone, while that by R1 produced by acupuncture point stimulation was partially antagonized by naloxone and dexamethasone, and that by non-acupuncture point stimulation was completely antagonized by dexamethasone, not by naloxone. In present experiment, the possibility that morphine tolerance may develop in naloxone reversal pathways not in dexamethasone reversal pathway of R1 and R2 pathways was examined. Pain threshold was measured by tail-flick latency of rats. Intraperitoneal dexamethasone (0.4 mg/kg 24 hours, 0.2 mg/kg 1 hour before morphine injection) had no effect on intraperitoneal 0.5 mg/kg morphine analgeisia which is equivalent to acupuncture analgesia. Morphine (0.5 mg/kg i, p.) caused analgesia in R1 pathway after lesion of 1-CM and the lateral septum (1-SP) which had been identified as belong to R2 pathway. Naloxone (1 mg/kg i, p.) partially antagonized this analgesia. Morphine analgesia caused by R1 pathway was slightly reduced after treatment of large doses of morphine (50 mg/kg, first day and 100 mg/kg morphine every 10 days) . Analgesia caused by non-acupuncture point stimulation after lesion of both 1-CM and 1-SP was not influenced by treatment of large doses of morphine. From these results, it was concluded that 1) morphine analgesia was caused by R2 pathway even in the presence of both analgesia inhibitory system (1-CM) and R1 pathway. 2) After lesion of both R2 and 1-CM, morphine caused analgesia by R1 pathway. This analgesia was partially antagonized by naloxone. 3) Morphine tolerance slightly developed in R1 pathway. 4) Analgesia caused by non-acupuncture point stimulation was not influenced by enough doses of morphine to develop morphine tolerance.
学校法人昭和大学・昭和医学会の論文

モルヒネ耐性の形成で区分される針鎮痛発現系と鎮痛抑制系で抑制されている鎮痛発現系

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