中枢去甲肾上腺素和强啡肽A(1-17)在痛觉调制中的相互作用  被引量:5

INTERACTION BETWEEN CENTRAL NOREPINEPHRINE AND DYNORPHIN A(1-17) IN PAIN MODULATION

在线阅读下载全文

作  者:董艺娜[1] 明晓云[2] 韩济生[1] 

机构地区:[1]北京医科大学神经科学研究中心,北京100083 [2]山东泰山医学院生理教研室

出  处:《中国疼痛医学杂志》1997年第1期38-41,共4页Chinese Journal of Pain Medicine

基  金:国家自然科学基金;美国国立卫生院DNA基金

摘  要:大鼠以辐射热甩民法测痛。应用脊髓蛛网膜下腔(i。t.)连续累加注射法观察药物的镇痛作用。(1)i.t.单独注射强啡肽A(1-17)2.5μg本身无镇痛作用,但与去甲肾上腺素(NE)合用时却能产生协同镇痛作用;该作用既能被i.t.注射α受体括抗剂酚妥拉明30μg所对抗,也能被k阿片受体桔抗剂Nor-BNI9μg所对抗。(2)强啡肽A和NE的协同镇痛提示在两种受体激动剂协同作用时,阻断其中一种受体,即能据抗其协同镇痛作用。(3)酚妥拉明可对抗强啡肽镇痛,Nor-BNI可对抗NE镇痛,表明强啡肽与NE的脊髓镇痛机制并非简单的串联或并联关系,两者有可能存在一个环路联系。Nociception of the rat was assessed by measuring the latency of tail flick response .induced by thermal irradiation. Receptor agonists and antagonists were administered intrathecally (i- t. ) in serially increasing doses. The results are as follows: (1 ) I- t. injection ofsubthreshold dose (2. 5μg) of kappa receptor agonist dynorphin A(1- 17) produced noanalgesic effect by itself, yet it potentiated the analgesic effect of NE administered i. t. (2)The Synergistic effect produced by i. t. injection of dynorphin A(1-17) and NE could beblocked by i. t. injection of either alpha receptor antagonist phentolamine (30μg) or the kappa antagonist Nor- BNI (9μg), suggesting that the synergistic analgesia seems to depend onthe co-activation of alpha and kappa receptors. Blockade of any one of them leads to a totalabolishment of the synergistic effect. (3 ) Analgesic effect produced by dynorphin A(1-17 )(11μg, i. t. ) could be blocked by α-receptor antagonist phentolamine (30μg, i. t. ) and theanalgesia produced by NE could be blocked by K-antagonist Nor-BNl (9μg, i. t. ). The results suggest that the relations between dynorphin and NE may not be simply parallel or serial, but presumably in a form of circular or loop connection .

关 键 词:去甲肾上腺素 强啡肽A 镇痛 痛觉 

分 类 号:R338.3[医药卫生—人体生理学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象