大白鼠足三里電針止痛的中樞機轉：腦下垂體的C14 去氧葡萄糖代謝功能研究

Pituitary Functional Image Pattern Associated with the Mechanism of the Tsu-San-Li Electroacupuncture Produced Analgesia in Rats: A[fed8] C-2DG Study

痛覺是由許多不同層面的感覺傳入，經過認知徑路（包含身體的壓抑調節系統亦即內分泌、免疫、自主神經、和嗎啡系統）的調控，產生痛的感覺和行為反應（MelZack, 1999 ）。我們早先的研究結果（Huang, 1988 ）顯示大白鼠足三里低頻電針止痛的的中樞機轉是經由活化：1） 內生性止痛系統；2） 內生性嗎啡系統（endogenous opioid system ），如下視丘室旁核、弓狀核、及腦下垂體前葉；3） 邊緣情緒系統，進而活化，引起止痛作用。腦下垂體是一個神經內分泌機制的調控關鍵器官，負責維持恆定、代謝能量、生殖、成長、泌乳等功能。為了解腦下垂體在低頻電針止痛中所扮演的角色，本研究藉由評估腦下垂體的葡萄糖代謝功能表現，並以dexamethasone 阻斷腦下垂體前葉corticotrophs 釋放ACTH/β-endorphin ，來探討此一問題。結果顯示dexamethasone 有效阻斷低頻電針止痛，使閃尾反應的延長時間從打藥前的25 % 降低為1% 。因此我們推斷ACTH/β-endorphin 參與低頻電針止痛作用。再者，電針 + 痛刺激組的腦下垂體葡萄糖代謝功能表現順序為 “ 中葉 > 後葉 = 前葉” 與對照組的葡萄糖代謝功能表現順序“ 後葉 > 前葉 > 中葉” 不同。電針 + 痛刺激組在後葉靠近中葉的葡萄糖代謝功能增加，且後葉葡萄糖代謝功能下降，推測與低頻電針止痛減低壓力作用有關。The multiple factors contributing to the output pain experience and behavior include the activity of the body's stress-regulation systems, including cytokines as well as the endocrine, autonomic, immune and opioid systems. In a previous report we found that 2 Hz electro- acupuncture-analgesia (EAA) activated glucose utilization of brain structures involved with: 1) multiple endogenous analgesia systems; 2) anti-inflammatory response and blood-pressure regulating properties (anterior and posterior pituitary); and 3) affective responses (limbic system) associated with pain and analgesia. The Pituitary gland is a critical organ of the neuroendocrine system and is essential for the maintenance of homeostasis, metabolism, reproduction, growth, and lactation. In order to know the role of the pituitary in the 2 Hz EAA, we evaluated the metabolic changes and patterns of the pituitary as related to the thermal tail-flick pain stimulation and the EAA. Dexamethasone was used to inhibit the ACTH release from the pituitary by a negative feedback mechanism. As a result, we demonstrated that 2 Hz EA at T-S-L acupoint induced analgesic effect which was verified by a 25 % elongation of the mean tail-flick latency (MTLF) and that dexamethasone blocked this EAA effect with only a 1 % MTLF elongation. Since ACTH and β-endorphin are co-released from the anterior pituitary lobe corticotrophs, the blockade of EAA by dexamethasone may indicate the involvement of β-endorphin. In addition, we found that in the “Pain+EA” group, the pituitary labeling pattern showed an unusual pattern with the greatest amount of labeling present in the intermediate lobe, followed by lesser but equal amounts in the posterior and anterior lobes, i.e., INP > POP = ANP, which was in contrast to the pattern in the control group of “POP > ANP > INP”. In both the “Pain” and “Dexa+Pain+EA” groups, the pituitary labeling showed the same trend in LCGU values as that of the control group, i.e., POP > ANP > INP. This difference in labeling patterns of the posterior lobe appeared to be correlated with the EAA effect.