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作 者:潘玉贞[1] 王丽华[1] 唐毓环[1] 尹宪明[1] 王绍[1]
机构地区:[1]白求恩医科大学生理教研室
出 处:《生理学报》1992年第4期326-332,共7页Acta Physiologica Sinica
摘 要:通过埋植套管向大鼠双侧缰核分别注射0.1mol/L CaCl_2 0.5μl,0.06mol/L ACh0.5μl,5.4×10^(-3)mol/L三碘季铵酚0.5μl和14.4×10^(-3)mol/L阿托品0.5μl后观察到,Ca^(2+)降低基础痛阈并拮抗电针镇痛效应;ACh拮抗电针镇痛;Ca^(2+)拮抗电针镇痛的作用可被胆碱能N受体阻断剂三碘季铵酚完全翻转。提示缰核内的Ca^(2+)可能通过ACh实现其拮抗电针镇痛的效应。0.1 mol/L CaCl_2 0.5 μl, 0.06 mol/L ACh 0.5 μl, 5.4×10^(-3) mol/L gal-lamine triethiodide (cholinergic nicotinic receptor blocker) 0.5 μl and 14.4×10^(-3)mol/L atropine (cholinergic muscarinic receptor blocker) 0.5 μl were injectedthrough bilateral intracranial cannulae in rat habenula. Pain threshold wasmeasured by the latency of tail-flick reflex elicited by radiant heat exposure beforeand after intracerebral injection. CaCl_2 significantly reduced the basic painthreshold and weakened the effect of the acupuncture analgesia. ACh apparentlyantagonized the effect of acupuncture analgesia. Gallamine triethiodide couldrecover the pain threshold almost to the raised level by acupuncture, butatropine only strengthened the effect on pain threshold weakly and briefly.The results suggest that the antagonistic effect of Ca^(2+) may be mediated via AChin habenula.
分 类 号:R338.26[医药卫生—人体生理学]
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