Abstract
Stress induced analgesia (SIA) producing central pathway was explored by comparing it with that of‘so called’acupuncture analgesia (AA) caused by acupuncture point stimulation and that of acupuncture non-point stimulation produced analgesia (NAA), which appeared after lesion of the analgesia inhibitory system, the lateral centromedian nucleus of thalamus (ICM) . Tail flick latency of Wistar rats was used for measurement of pain threshold. Electric stress shock of 1 sec duration was applied between back and upper thigh at 1/5 sec. The stimulus strength was increased from 1.5 mA to 3 mA within 10 min onset of stimulation. Acupuncture point and non-point stimulation were applied to the anterior tibial muscle and the abdominal muscle, respectively, with a stimulus strong enough to cause slight muscle contraction. Lesions of the dorsal and lateral periaqueductal central gray (dPAG and IPAG) and ICM were made by electrode insertion. SIA, caused by electric shock in the present experimental, reached a maximum at 30 min after onset of stimulation and then decreased gradually. Analgesia remained after of stimulation (after effect) . Such SIA was abolished by hypophysectomy, naloxone (1 mg/kg i. p.) or dexamethasone (0.4 mg/kg 24 hr. before, and 0.2 mg/kg 1 hr. before) . Individual variation was observed in SIA, but this variation has no correlation with that of AA. SIA was not influenced by lesion of the dPAG, which is the site of the afferent analgesia-producing pathway in AA from acupuncture point to the hypophysis, or by intrathecally applied naloxone (0.2 μg), which abolished AA. Four days were necessary to recover normal SIA. SIA had no effect on AA for 4 days after after SIA. Like NAA, SIA was abolished by lesion of the 1PAG, however, 1CM lesion, by which NAA was induced by acupuncture non-point stimulation, did not produce SIA in SIA non-effective animals. Analgesia was induced after 1CM lesion by weak stress shock, which did not produce SIA. This analgesia was not antagonized by naloxone. NAA was not influenced by SIA for 4 days. Since 1) SIA was antagonized by either naloxone or dexamethasone, while AA was antagonized only by naxolone and NAA only by dexamethasone, 2) SIA had no effect on AA or NAA for 4 days, were necessary to recover SIA, 3) dPAG lesion or intrathecal naloxone, which abolished AA, had no effect on SIA, therefore, it was concluded that the central analgesia producing pathway for SIA is different from that of AA or NAA.
