Abstract
According to our previous experiments, analgesia was not produced by stimulation of the non-acupuncture point with same intensity and frequency of acupuncture point stimulation, and that same stimulation of the non-acupuncture point induced an analgesia after lesioning of the analgesia inhibitory system (AIS) such as lateral centro-median nucleus of the thalamus (L-CM) and of the part of the posterior hypothalamus (I-PH) . Similar results were obtained after treatment of D-phenylalanine (DPA) . However it is not known whether DPA directly inhibits the AIS or DPA antagonizes the inhibitory transmitter of the AIS in the lateral periaquaductal central gray (L-PAG), which was found as the inhibition acting site from AIS on the pathway connected to the non-acupuncture point. In present experiment, the non-acupuncture point stimulationproduced-analgesia was examined by micro-injection of DPA into the L-CM, I-PH and L-PAG to find out the manner of the DPA action on the AIS, observing the tail flick latency of rats as the index of the pain threshold. Non-acupuncture point stimulation-produced-analgesia was induced after micro-injection of DPA (84 ng) into the L-CM or I-PH, while such analgesia was not produced after injection of DPA to the L-PAG. Therefore DPA directory inhibits the AIS. It was reported that proglumide, antagonist of cholecystokinin, potentiates morphine analgesia. After treatment of intra-peritoneal 20 μg/kg proglumide, analgesia was produced by non-acupuncture point stimulation. Same kind of analgesia was also produced by microinjection of proglumide (5-8 ng) into the L-CM and I-PH and not by application to the L-PAG. From these results it was concluded that both DPA and proglumide inhibit the AIS directly and it was strongly suggested that cholecystokinin acts as the transmitter in the AIS. Relation between DPA and proglumide is not known yet.
