摘要
采用离体灌流背根节 (dorsalrootganglion ,DRG)和单纤维记录神经元自发放电的方法 ,观察到育亨宾对受损DRG神经元的自发放电呈现兴奋作用 ,并初步研究了其发生机制。用外源性育亨宾 (10 μmol/L)灌流损伤的DRG时 ,在 2 2个有自发放电的DRG神经元中 ,有 18个神经元产生明显反应。育亨宾对损伤神经元自发放电的兴奋作用 ,可被α1 肾上腺素能受体拮抗剂哌唑嗪 (5 μmol/L)明显阻断。用 6 羟多巴胺化学性交感神经切断和胍乙啶耗竭交感末梢后 ,育亨宾的兴奋作用均明显减小。结果表明 :育亨宾阻断交感节后神经末梢上的α2 肾上腺素能受体 ,引起去甲肾上腺素 (norepinephrine,NE)的释放 ;释放的NE作用于损伤DRG神经元上的α1 肾上腺素能受体 ,而对受损神经元自发放电呈现兴奋作用。提示交感节后神经末梢可能存在一种持续性抑制NE释放的新机制 。
With methods of the perfusion of dorsal root ganglia (DRGs) in vitro and single fiber recording of the spontaneous activity,the excitatory effect of yohimbine on injured sensoryneurons was observed and its preliminary mechanisms were further investigated in this study. Eighteen out of the 22 neurons responsed to yohimbine (10 μmol/L) perfused to injured DRGs, and the excitatory effect was blocked by α 1 adrenoceptor antagonist, prazosin (5 μmol/L). Moreover, the excitation was dramatically attenuated following chemical sympathectomy with 6 OHDA and depletion of sympathetic terminals with guanethidine.The above results suggest that yohimbine blocks α 2 adrenoceptor at postganglion sympathetic endings and causes the release of norepinephrine (NA), which acts on α 1 adrenoceptor in DRG neurons, thereby exerting an excitatory effect on the spontaneous activity in injured neurons. There might be a novel way in postganglion sympathetic terminals that persistently prevented NA release without the control of postganglion sympathetic ganglia and action potential.
基金
国家自然科学基金 ( 30 0 30 0 40 )
"脑功能和脑重大疾病的基础研究"(G19990 5 40 0 4)
