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. The relation of the pituitary gland to production of AA and NAA was investigated with regard to the neuronal mechanism previously observed in the arcuate nucleus. We showed, at that time, that the final sector of the path from the acupuncture point to the pituitary gland is in the medial part of the hypothalamic arcuate nudes (M-HARN), AA is produced by activation of the descending pain inhibitory system (DPIS), and the initial sector of the DPIS is in the posterior part of the hypothalamic arcuate nucleus (P-HARN) . Pain threshold was measured by rat tail flick latency (TFL) . Drugs were applied through fine cannulae inserted into the brain. β-Endorphin, ACTH or dopamine microinjected into the P-HARN produced analgesia dose, dependently. Analgesia of β-endorphin disappeared, and analgesia of ACTH and dopamine were unchanged after denervation of the M-HARN. Lesioning the anterior part of the hypothalamic arcuate nucleus (A-HARN) abolished NAA and analgesia produced by stimulation of the anterior hypothalamus (NAA-AH), which was previously thought to be the final sector of the NAA pathway to the pituitary gland was abolished by lesion of the A-HARN, and potential was evoked in the A-HARN by stimulation of the non-acupuncture point and of the NAA-AH. Thus the A-HARN was more rostrally located than the NAA-AH in the NAA afferent pathway. Analgesia of ACTH microinjected into the P-HARN was abolished, while that of dopamine or β-endorphin was not changed after denervation of the A-HARN. Lesion of the median eminence (ME) abolished AA, but stimulation of ME did not produce analgesia. Potential was evoked in the ME by stimulation of the acupuncture point (tibial muscle) . From these results it was concluded that there is dopaminergic transmission between the M-HARN and P-HARN in AA, and between the A-HARN and P-HARN in NAA, and this transmission might be present only in the presence of presynaptic action of βendorphin or ACTH released from the pituitary gland.
