Morphine analgesia mediated by activation of the acupuncture-analgesia-producing system.

Analgesia caused by intraperitoneal 0.5 mg/kg morphine (MA) in rats is equivalent to acupuncture analgesia (AA) caused by low frequency stimulation of the tibial muscle (Tsusanli acupuncture point). Analgesia equivalent to both AA and MA was produced by intrathecal application of 0.05 microgram morphine. This analgesia exhibits individual variation in effectiveness which is parallel to those of both AA and MA, and disappears after 250 mg/kg intraperitoneal D-phenylalanine. Analgesia that persisted after termination of acupuncture stimulation was not affected, maximally developed MA and AA were both partially antagonized, and the initial development of AA and MA were completely antagonized by intrathecal application of 0.2 microgram naloxone. Analgesia caused by intrathecal 0.05 microgram morphine was abolished by bilateral lesion of the anterolateral tract (ALT) of the spinal cord and that caused by acupuncture stimulation was abolished by contra-lateral lesion. Analgesia caused by larger doses (0.1-0.2 microgram) of intrathecal morphine was not abolished, but persisted after ALT lesion, unilateral lesion of the dorsal periaqueductal central gray (D-PAG), or hypophysectomy. Potentials were evoked by acupuncture stimulation in the bilateral D-PAG. Analgesia produced by D-PAG stimulation was not affected by ALT lesion nor by intrathecal naloxone, but was abolished by lesion of the dorsolateral funiculus. These results imply two types of morphine action in the spinal cord to produce analgesia: activation of the ascending AA pathway; and direct inhibition of pain message in the spinal cord. They also show that the AA producing pathway ascends contralaterally in the ALT and then bilaterally in the D-PAG.