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Brain Res Bull. 1992 Mar; 28(3): 379-91.

Analgesia inhibitory system involvement in nonacupuncture point-stimulation-produced analgesia.

Takeshige C, Kobori M, Hishida F, Luo CP, Usami S.

Department of Physiology, Showa University School of Medicine, Tokyo, Japan.

Acupuncture analgesia (AA), caused by low-frequency stimulation of an acupuncture point (AP)--in this case the tibial muscle--was augmented. Nonacupuncture analgesia (NAA), caused under certain circumstances by stimulation of a nonacupuncture point (NAP)--in this case the abdominal muscle--was unmasked by lesion in the lateral centromedian nucleus of the thalamus (L-CM) or part of the posterior hypothalamus (I-PH). Stimulation in these regions suppressed the augmented part of the AA and blocked the NAA. These regions were, collectively, given the name analgesia inhibitory system. NAA was abolished, the same as AA, by hypophysectomy. The pathways from the AP and NAP to the pituitary gland were different. AA was naloxone reversible, and NAA was dexamethasone reversible. The analgesia inhibitory system is activated nonspecifically by stimulation of either an AP or NAP. It ascends to the I-PH, thence to the L-CM, and ultimately inhibits the pathway nonspecifically connected to the NAP and AP in the lateral part of the periaqueductal central gray (PAG), without affecting the pathway specifically connected to the AP. Thus, only stimulation of an AP will produce analgesia, whereas stimulation of an NAP will not normally produce analgesia. Stress-induced analgesia (SIA) is produced in a different way than AA or NAA.

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