Abstract
It was found previously that analgesia caused by low frequency stimulation of the tibial muscle, which is corresponded to the Tsu-sanli acupuncture point (AA), and analgesia caused by similar stimulation of the abdominal muscle, which is correspond to the non-acupuncture point (NAA), after lesion of the lateral neutromedian nucleus of the thalamus which is the region belong to the analgesia inhibitory system, were abolished by hypophysectomy and that both analgesia were finaly produced by activation of the descending pain inhibitory system (DPIS) which might be activated by some neuro-hormonal factor liberated from the pituitary gland. In present experiment, it was undertaken to know whether the pituitary hormonal factor acts as the direct activatior of the DPIS or it coactivates DPIS with that of adrenal gland Hence, successive changes of AA and NAA after ablation of pituitary or adrenal gland were observed. Pain threshold was measured by the tail flick latency (TFL) of the rats and analgesia was denoted by percent increase of TFL. Pituitary gland was removed by trans-auricular method and the adrenal gland was removed under laparotomy. As the results, AA augemented 6 hours after removal of the pituitary or adrenal gland, and abolished 12 hours after removal. Augemented AA 6 hours after removal of these glands was not antagonized by naloxone (1mg/kg i, p.) nor by dexamethasone, but was abolished by lesion of the dorsal part of the periaqueductal central gray which is the region of the pathway from the acupuncture point to the pituitary gland and was partialy antagonized by methysergide (2mg/kg i, p.) as Obserred in control AA. NAA also augemented 6 hours after removal of pituitary or adrenal gland. Unlike AA, augemented analgesia in NAA remanined 18 hours after hypophysectomy and the reduced analgesia remained same hours after removal of adrenal glands. In both cases analgesia was abolished 24 hours after removal. 0.75-10mg/kg corticosterone did not restore the abolished analgesia 1 week after removal of adrenal gland. Evoked potential in the arcuate nucleus of the hypothalamus, which is the initial region of the DPIS, caused by stimulation of the anterior hypothalamus, which is the final neuronal region of the pathway from the acqpuncture point to the pituitary gland, was not influenced by removal of adrenal gland. It was conclued that the humoral factor from the pituitary gland might coactivate with that of the adrenal gland to produce AA and NAA. The intrinsic mechanism to cause the augemented AA and NAA in absence of the pituitary and adrenal glands, is not known yet.
