Abstract
Hypophysectomy abolished analgesia induced by low frequency non-acupuncture point (abdominal muscle) stimulation (NAA) after lesioning the analgesia inhibitoty system (AIS), including the lateral part of the centromedian nucleus of the thalamus (L-CM), or treatment with the cholecystokinin (CCK) antagonist, proglumide. Relations between the arcuate nucleus (HARN) and the pituitary gland in production of NAA were investigated by change of pain threshold in the tail flick test, and of neuronal activity in the posterior part of the HARN (P-HARN) . Analgesia was produced dose-dependently by ACTH i.p. (ED50=0.25 mg/kg) . Firing rates of P-HARN neurons were increased by non-acupuncture point stimulation (HAPS) after lesioning the L-CM or treatment with 20ug/kg, proglumide i.v. Intravenous ACTH (0.25 mg/kg) increased the firing rates of P-HARN neurons that were also facilitated by NAPS after pretreatment with 20 μg/kg proglumide, i.v. Increment of the firing rates of P-HARN neurons by NAPS was antagonized by 0.6 mg/kg dexamethasone, i.v. The NAPS responsive neurons also responded to 0.1 mM dopamine ultramicroinjected into the neuronal recording site by picospritzer, but did not respond to 0.1 mM ACTH. Analgesia and increment of firing rates of the P-HARN neurons caused by NAPS or 0.25 mg/kg ACTH were abolished by hypophysectomy. Under these conditions, analgesia and increased firing rates were restored by concurrent application of NAPS and ACTH. It was concluded that NAA is produced by dopaminergic transmission between the anterior part of the HARN, which had previously been identified as the final section of the NAA afferent pathway to the pituiary gland, and the P-HARN in the presence of ACTH liberated from the pituitary gland by NAPS.
