Abstract
It was found previously in our labolatory that the centromedian nucleus of the thalamus (L-CM) was considered belonging to an analgesia inhibitory system since 1) lesion of the L-CM enhanced acupuncture analgesia (AA) caused by low frequency stimulation of the tibial muscle of rats, which was measured by tail flick test, 2) this stimulatron produced analgesia in the abolished AA after lesion of AA producing afferent pathway, which initiated from the tibial muscle and reached to the hypophysis, and 3) the same stimulation of the abdominal muscle did not produce analgesia in normal condition but produced analgesia after lesion of the L-CM. It was also found that D-phenylalanine (DPA) acts just like as lesion of the L-CM. In present experiments, it was examined by lesion and stimulation experiments of the posterior hypothalamus that the part of the posterior hypothalamus acts as an analgesia inhibitory system like L-CM. The effect of DPA on analgesia inhibition by stimulation of the analgesia inhibitory system was also examined. The restricted lesion of the part of the posterior hypothalamus (PH) by means of electrode insertion produced two kinds of changes in AA and morphine analgesia, which was caused by intraperitoneal 0.5mg/kg morphine and was equivalent to AA. One is enhancement of analgesia, and the other is little change of analgesia. Stimulation of the PH through inserted electrode for lesion inhibited the enhanced part of analgesia and the non-enhanced analgesia during stimulation, which were largely antagonized by dexamethasone applied 0.4mg/kg 24 hours and 0.2mg/kg 2 hours before experiment, and remaining analgesia was antagonized by 1 mg/kg naloxone, while it was found previously that AA was antagonized by naloxone, not by dexamethasone. Since all these results were same as those obtained after L-CM lesion, it was obvious that I-PH acts as the analgsia inhibitory system like L-CM, and that encancement of analgesia was the result of lesion of analgesia inhibitory system and non-enhanced analgesia was the results of both lesions of analgesia inhitory system and AA producing afferent pathway in the posterior hypothalamus. The complete inhibition of analgesia caused by I-PH stimulation was antagonized by pre-treatment of 250mg/kg DPA. Therefore it was concluded that inhibitory action of analgesia inhibitory system was antagonzed by DPA.
