低頻電針止痛引起老鼠中樞內生嗎啡系統葡萄糖代謝率的改變

Metabolic Changes in the Rat CNS Endogenous Opioid Systems Associated with Electroacupuncture-Produced Analgesia

大白鼠（雄300 - 500g）13隻分成四組，在靜脈注射C14去氧葡萄糖(C14-2DG)的同時分別給予不同的體感覺刺激45分鐘：對照組(n=3)間歇性溫(400。C)尾端刺激：“痛＂刺激組(n=4)：間歇性（每隔30秒一次）熱水(560。C)尾端刺激；“痛＂刺激＋電針(2Hz)組(n=3)：56。C熱水尾端刺激＋電針(2Hz)足三里，電針(2Hz)組(n=3)：電針足三且，止痛效果是以閃尾反應時間來判定。中樞系統神經核代謝功能的變化是用Sokoloff et al., (1977 )之定量去氧葡萄糖方法來評估。“痛＂＋電針組對56。C熱水刺激的平均閃尾時間(MTFL)由2.61秒（電針前）增到3.66秒（電針後）肯定了電針(2Hz)足三里產生的止痛效果。與對照組比較，“痛＂＋電針組外側網狀核(LRN)，下視丘弓狀核(ARC)，室旁核(PVH)，外側瞳核(HB )，丘腦前腹側前內側核(AV&AM)，後扣帶回(PCG)，內側乳頭體(MEM)和腦下垂前葉(ANP)的葡萄糖代謝率(LCGU)有顯著增加(p< 0.05)；然而“痛＂刺激組則只有ARC，AV & AM及PCG的LCGU有顯著增加(p< 0.05 )。綜合上述結果，得到結論：低頻(2Hz)電針（足三里）止痛乃是經由活化了中樞神經的三個內生性嗎啡系統：POMC (Proopiomelanocortin)系統(ANP,ARC, LRN)；Proenkephalin( MEM,LRN, PVH)；和Prodynorphin ( MEM, AV & AM, PCG, HB )所引起。

Thirteen adult male Sprague-Dawley rats received one of four different somesthetic stimuli for 45-minutes following an injection of (14C)-2-deoxyglucose (2DG): 1. Non-noxious (40℃ water) distal-third of tail stimulation (Control, n=3); 2. Noxious stimulation (56℃ water) of the distal-third of tail (”Pain”, n=4); 3. Paired noxious tail stimulation and electroacupuncture (EA) (2Hz) of right Tsu-San-Li point (proximal anterior tibial muscle) (”Pain” + EA, n=3); and 4. EA stimulation of right Tsu-San-Li (EA, n=3). Efficacy of noxious thermal and EA stimuli was determined by measuring Tail-flick Respones Latencies. Quantitative 2DG method of Sokoloff et al. (1977) was used to assess functional changes in the central nervous system. The increased Mean Tail-flick Latency (MTFL) in ”Pain” + EA group from 2.61 sec (before EA) to 3.66 sec (after EA) indicated that EA was effective in producing analgesia. In comparison with the Control group, LCGU's in the ”Pair” +EA group were significantly increased (p＜0.05) in the following nuclei: Lateral Reticular nucleus (LRN); Arcuate nucleus (ARC); Paraventricular nucleus of hypothalamus (PVH); Lateral Habenular nucleus (HB); Anteroventral and Anteromedial nuclei of thalamus (AV & AM ); Posterior Cingulate Gyrus (PCG); Medial Mammillary nucleus (MEM) and Anterior Pituitary (ANP). LCGU's in ARC, AV & AM, PCG of the ”Pain” group, however, were significantly increased (p＜0.05 ) in comparison with control groups. In conclusion, EA under the above stimulus conditions activates structures involved with portions of three endogenous opioid analgesia systems 1. Proopiomelanocortin (ANP, ARC, LRN), 2. Proenkephalin (MEM, LRN, PVH), and 3. Prodynorphin (MEM, AV & AM, PCG, HB) derived peptide containing immunoreactive nuclear groups.