Abstract
As previously reported, acqunceure analgesia caused by 1 Hz repetitive stimulation of the tibial muscle of rats was abolished by hypophysectomy, and the pathway from the tibial muscle as an acupuncture point to the hypophysis was defined as the acupuncture afferent pathway, and the pathway of the descending pain inhibitory system activated by some unknown substances liberated from the hypophysis was defined as the acquncture efferent pathway. Acupuncture stimulation was not always effective to produce analgesia in every animal. Animals are able to be classified into responder or nonresponder by a significant increase (p<0.05) of tail flick latency. Stimulation-produced-analgesia of the raphe magnus (RM) was different between responder and non-responder. In present experiments, involvement of the acupuncture afferent and efferent pathways in the reticular gigantocellular nucleus (NRGC) and the reticular paragigantocellular nucleus (NRPG) was examined by stimulation-produced-analgesia (SPA) of these regions and by microinjection of morphine. SPAS of the NRGC and NRPG were different between responder and non-responder. SPA of the responder lasted for several minutes after termination of stimulation, while that of the non-responder was limited only during stimulation. After lesion of the dorsal part of the periaqueductal central gray (D-PAG) which was identi-fied as the acupuncture afferent pathway, the character of SPA of the responder changed to that of non-responder which was not influenced by lesion of the D-PAG. SPA after D-PAG lesion was abolished by intrathecal 20μg phentolamine, a noradrenergic antigonist. Microinjection of morphine (0.5, μg/μl) into the NRGC and NRPG produced different analgesia in responder and non-responder. Analgesia was only produced in the responder by NRGC microinjection of morphine, but not in the non-responder. This analgesia was abolished by D-PAG lesion. On the ther hard, almost similar analgesia was produced by NRPG morphine microinjection in both responder and non-responder. Analgesia caused by 2μg/μl morphine injection to the NRGC was different between responder and non-responder. Analgesia in the responder was developed rapidly while that of the non-responder was developed slowly. After lesion of the D-PAG, rapidly developed analgesia dispppeared and analgesia changed to that of non-responder which was not influenced by D-PAG lesion. Remaing analgesia after lesion of D-PAG was abolished by 40μg intrathecal phentolamine. Microinjection of 5μg morphine to the RM did not produce analgesia. It was concluded that both acupunctre afferent and efferent pathways were activated by stimulation of the NRGC and NRPG, while opiate receptor containing afferent and efferent pathways were found in the NRGC and NRPG respectively.
