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本研究观察到育亨宾对受损背根节 (DRG)神经元呈现兴奋作用 ,并初步研究了其发生机制。用外源性育亨宾 (10μmol/L)灌流损伤 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的兴奋作用可被α1 -肾上腺素受体拮抗剂哌唑嗪 (5μmol/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。结果显示 :育亨宾阻断交感节后神经末梢上的α2 -肾上腺素受体 ,引起去甲肾上腺素 (NE)的释放 ;释放的NE作用于损伤 DRG神经元上的α1 -肾上腺素受体呈现兴奋作用。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 ,这种抑制作用不依赖交感节后神经节和动作电位的存在
In this study, we observed that yohimbine exerted an excitatory effect on DRG neurons and initially studied its mechanism. When DRG was infiltrated with exogenous yohimbe (10μmol / L), 18 neurons in 22 DRG neurons with spontaneous discharge produced a significant response. The excitatory effects of yohimbin on injured neurons were significantly blocked by α1 - adrenergic receptor antagonist prazosin (5μmol / L). The excitatory effects of yohimbine were significantly reduced after chemical sympathectomy with 6 - hydroxydopamine and the depletion of sympathetic terminals with guanethidine. The results showed that yohimbin blocked the α2 - adrenergic receptor on the nerve endings of sympathetic postganglionic node and caused the release of norepinephrine (NE); the released NE acted on the α1 - adrenergic receptor on DRG neurons Showing excitement. Suggesting that post-sympathetic postganglionic nerve endings may have a sustained inhibition of NE release of new mechanisms, this inhibitory effect does not depend on the sympathetic postganglionic ganglion and the existence of action potential