Differentiation between acupuncture and non-acupuncture points by association with analgesia inhibitory system.
Acupuncture and non-acupuncture points were differentiated by their connection to different pathways in the central nervous system. We have found that the pathway connected to the acupuncture point is different from the pathway connected to the non-acupuncture point. In addition, pathway connected to the non-acupuncture point is inhibited within the lateral periaqueductal gray when the analgesia inhibitory system (AIS) is activated. We have explored these pathways by means of selective lesioning of discrete brain regions, selective stimulation of brain regions, as well as by recording evoked potentials arising from stimulation of acupuncture and non-acupuncture points. It was found that the lateral centromedian nucleus of the thalamus and the posterior hypothalamus are parts of the AIS. The acupuncture (tibialis muscle) and non-acupuncture (abdominal muscle) points are both connected to the AIS. Analgesia caused by stimulation of the acupuncture point is naloxone reversible, while that caused by stimulation of the non-acupuncture point after lesion of AIS is dexamethasone reversible. Stress-induced analgesia caused by low frequency electrical shock is naloxone as well as dexamethasone reversible. All three kinds of analgesia were abolished by hypophysectomy. The features and the degree of analgesia caused by intraperitoneal 0.5 mg/kg morphine were similar to analgesia caused by acupuncture point stimulation. D-phenylalanine acts like a lesion of AIS in analgesia caused by stimulation of acupuncture and non-acupuncture points, and enhances naloxone reversible analgesia. The descending pain inhibitory system plays a role as the common pathway to produce these three kinds of analgesia. This pathway is found in the arcuate nucleus (dopaminergic), ventromedian nucleus of the hypothalamus, raphe nucleus (serotonergic), reticular gigantocellular nucleus (noradrenergic) and reticular paragigantocellular nucleus.
Takeshige
C
C
D015670:Acupuncture Therapy / Q000379:methods*; D000818:Animals; D001921:Brain / Q000502:physiology*; D003907:Dexamethasone / Q000494:pharmacology; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects; D007034:Hypothalamus, Posterior / Q000502:physiology; D009020:Morphine / Q000494:pharmacology; D009270:Naloxone / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects; D009619:Nociceptors / Q000502:physiology*; D010487:Periaqueductal Gray / Q000502:physiology; D010649:Phenylalanine / Q000494:pharmacology; D010902:Pituitary Gland / Q000502:physiology; D011817:Rabbits; D051381:Rats; D011919:Rats, Inbred Strains; D012684:Sensory Thresholds / Q000187:drug effects; D013787:Thalamic Nuclei / Q000502:physiology
D009270:Naloxone; D010649:Phenylalanine; D009020:Morphine; D003907:Dexamethasone