Abstract
Analgesia caused by low frequency stimulation of the acupuncture point (AA), and of the non-acupuncture point after lesioning the analgesia inhibitory system (NAA), was abolished by hypophysectomy. We previously found that the final region of the AA afferent pathway from the acupuncture point to the pituitary gland was the medial part of the hypothalamic arcuate nucleus (M-HARN), and that of NAA afferent pathway was the anterior hypothalamus (NAA-AH) . The initial region of the descending pain inhibitory system involved in AA and NAA was the posterior part of the arcuate nucleus (P-HARN) which is located close to the M-HARN. Effects of 9-endorphin and of ACTH on the neural connection between M-HARN and P-HARN or NAA-AH and P-HARN were investigated to clarify relations between the pituitary gland and AA or NAA. Pain threshold was measured by rat tail flick latency (TEL) . Drugs were applied through fine cannulae to the brain. Animals were classified as responder or non-responder by the presence or absence of significant increase in TFL. Analgesia of the AA responder was not changed, but that of non-responder was changed to that of the responder by 0.5 mg/kg i.p, morphine which produced analgesia equivalent to AA. Naloxone microinjected into the P-HARN dose-dependently antagonized AA (ED50 =1.2 pg) and microinjected morphine (ED50 = 0.6 μg) or j3-endorphin (ED50 = 0.25 μg) dose-dependently produced analgesia and changed non-responders to responders. AA abolished by hypophysectomy was restored by 0.5 mg/kg morphine (i.p.), or morphine (0.5 μg) or 3-endorphin (0.1 μg) microinjected into the P-HARN during acupuncture point stimulation. Dexamethasone, injected i.p. or microinjected into the NAA-AH (ED50=0.12pg) or P-HARN (ED50=0.08 μg), antagonized NAA dose-dependently. ACTH microinjected into the NAA-AH (ED50=0.25 μg) or P-HARN (ED50=0.6 μg) dose-dependently produced analgesia. NAA abolished by hypophysectomy was restored by concurrent application of non-acupuncture point stimulation and ACTH (0.5 μg) microinjected into P-HARN but not into the NAA-AH.The dopamine antagonist, haloperidol, microinjected into the P-HARN antagonized both AA and NAA (ED50=0.35 μg), and dopamine microinjected into the P-HARN dose-dependently produced analgesia (ED50=0.5 μg) . These results imply that : 1) There should be a neural connection between the M-HARN and P-HARN in AA, between the NAA-AH and P-HARN in NAA, and the transmitter might be dopamine. 2) This neural transmission might be available only in the presence of jS-endorphin or ACTH associated with the pituitary gland mechanism. 3) μ-Endorphin and ACTH might act presynaptically in this neural transmission.
