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作 者:李韶[1] 吴晓平[2] 张自东[2] 崔存德[1]
机构地区:[1]滨州医学院生理教研室,山东滨州256603 [2]同济医科大学基础医学院生理学教研室,武汉430030
出 处:《针刺研究》1998年第1期16-30,共15页Acupuncture Research
摘 要:实验在60只SD大鼠上进行。采用细胞外记录方法,记录中脑导水管周围灰质(PAG)内痛兴奋神经元(PEN)的自发放电和伤害性刺激的诱发放电。主要观察中脑楔状核(NCF)内微量注射促甲状腺激素释放激素(TRH)和乙酰胆碱(ACh)对PAG内PEN的痛放电影响,以及TRH与NCF内胆碱能神经的关系。结果表明:(1)NCF内分别注入TRH(0.5μg/0.5μl)和ACh(2.5μg/0.5μl)均能明显抑制PAG内PEN的痛放电频率。而将等剂量TRH注入NCF背侧的下丘内,对PAG的痛放电则无明显影响。(2)预先注入阿托品(2.5μg/0.5μl)再注入TRH或ACh,阿托品能阻断ACh对PAG痛放电的抑制效应;但不影响TRH的抑制作用。(3)单独注入阿托品(2.5μg/0.5μl)对PAG的抑制效应也无明显影响。结果提示:外源性TRH和ACh都参与NCF对伤害性信息的调制作用,ACh的抑制效应是经m-受体介导的;而TRH的作用似乎与m-受体无关。Experiments were performed on 60 Sprague-Dawley rats. Using the extracellular recording method, We recorded the frequencies of spontaneous and evoked discharge of pain excitation neurons in the periaqueductal gray (PAG) to investigate the effects of TRH, ACh microinjected into nucleus cuneiformis(NCF) on the frequencies of evoked discharge of pain(PEN) and the relation of TRH to cholinergic nerve. The results as follows: (1) Injection of TRH(0. 5μg/0. 5μl, n = 12), ACh(2. 5μg/o. 5μl, n=11)into NCF could all suppress the frequencies of evoked discharge of PEN in PAG(P<0.001, 0.01, 0. 05), the maximal inhibitory rate was 77. 3±7. 5 % and 78. 4 ±7.0 % respectively. (2)Inhibitory effects of ACh (n = 5) could be antagonised by preinjection of atropine(2. 5μg/0. 5μl) into NCF(P < 0.05), but TRH(n = 6) not. (3) Atropine(2. 5μg/0.5μl, n = 8 ) injected into NCF could not significantly influence the evoked discharge of PEN in PAG. These findings suggest that some neurons in NCF might participate in the process to modulate noxious information transmission in CNS. TRH and ACh might be a neuromodulator or transmitter in the antinociception of NCF. The inhibitions of ACh may be mediated by cholinergic M-receptor. but TRH could not be mediated by cholinetgic Mreceptor.
分 类 号:R338.3[医药卫生—人体生理学]
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