Abstract
We found in our previous work that adrenalectomy abolished analgesia caused by low frequency stimulation of the acupuncture point (AA) as well as that caused by non-acu-puncture point (NAA) stimulation after lesioning of the analgesia inhibitory system. Since AA and NAA were abolished after adrenalectomy and abolished AA and NAA were not restored by corticosterone, and it has been reported that sodium ions are associated with opioid transmission, relations between sodium ions and adrenal gland functioning in production of AA and NAA were investigated in adrenalectomized rats. Pain threshold was measured by tail flick latency (TFL) . Concentration of sodium ions in the blood was measured by a Na-K analyzer. AA and NAA were abolished 12 and 24 hours after adrenalectomy, respectively, and 1-2ml of intraperitoneal or intravenous 5% NaCl restored abolished AA and NAA 1 hour after application. Potentials in the dorsal and lateral parts of periaqueductal central gray (D-PAG, L-PAG), evoked by stimulation of the acupuncture or non-acupuncture point, were abolished by adrenalectomy respectively, in 12 or 24 hours. These potentials were also restored by the same administrations of NaCl. Stimulation-produced analgesia in the D-PAG or L-PAG were abolished after adrenalectomy and were restored by NaCl. Abolished AA and NAA after hypophypectomy were restored by microinjecton of β-endorphin or ACTH to the posterior hypothalamic arcuate nucleus respectively. The restored AA and NAA were abolished again by adrenalectomy, and the abolished AA and NAA were restored by NaCl. AA and NAA, before their abolition after adrenalectomy, were not antagonized by naloxone or dexamethasone, respectively, unlike normal AA and NAA. The antagonistic action of naloxone and dexamethasone were restored by NaCI in adrenalectomized rats. The content of Na+ ions was restored gradually after adrenalectomy and this was recovered by NaCl application. These results indicate that 1) sodium ions are necessary for synaptic transmission associated with methionine-enkephalin in the spinal cord and, β-endorphin in the hypothalamus in AA, and dynorphin in the spinal cord and ACTH in the hypothalamus in NAA. These transmitters, associated with AA and NAA were investigated in our previous work. 2) Sodium ions are also necessary for the antagonists of these transmitters. 3) The amount of sodium ions needed was different between agonist of AA and of NAA and between antagonist and agonist.
