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目的：进一步研究损伤初级感觉神经元交感感觉偶联作用的神经机制． 方法：利用背根节（ Ｄ Ｒ Ｇ）慢性压迫模型，采用离体灌流 Ｄ Ｒ Ｇ 和单纤维记录神经元的自发放电． 结果：当外源性去甲肾上腺素（ Ｎ Ｅ， １０ μｍ ｏｌ／ Ｌ）浸浴损伤 Ｄ Ｒ Ｇ 时，在９５ 个神经元中有 ８５ 个有自发放电的神经元产生明显反应． ８５ 个神经元中， ４４ 个呈现单纯兴奋效应； ２１ 个表现先兴奋后抑制效应； ６ 个出现兴奋抑制交替振荡现象； １４ 个表现抑制效应． Ｎ Ｅ对损伤神经元的兴奋作用可分别被哌唑嗪（５μｍ ｏｌ／ Ｌ）和育亨宾（１０ μｍ ｏｌ／ Ｌ）部分阻断． 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， Ｎ Ｅ 对损伤 Ｄ Ｒ Ｇ神经元放电频率最大增加百分数明显增加． 结论：在 Ｄ Ｒ Ｇ 慢性压迫模型上，损伤的 Ｄ Ｒ Ｇ 神经元存在肾上腺素能敏感性；α１ 和 α２ 肾上腺素受体参与兴奋性肾上腺素能敏感性；这种肾上腺素能敏感性不依赖于交感节后神经末梢的存在．
Objective: To further investigate the neural mechanism of sympathetic sensory coupling injury primary sensory neurons. Methods: Spontaneous discharges of neurons were recorded by in vitro perfusion D RG and monofilament using chronic compression model of DRG. Results: When exogenous norepinephrine (N E, 10 μm ol / L) infiltrated the DRG, 85 of 95 neurons spontaneously discharged neurons produced significant responses. Of the 85 neurons, 44 showed a simple excitement effect; 21 showed excitatory and repressive effects; 6 showed excitement and suppressed the alternating oscillations; and 14 showed inhibitory effects. Excitatory effects of N E on injured neurons were partially blocked by prazosin (5 μmol / L) and yohimbine (10 μmol / L), respectively. With 6hydroxy dopamine chemical sympathectomy and guanethidine depletion of sympathetic terminals, N E significantly increased the maximum increase of the discharge frequency of damaged DRG neurons. CONCLUSION: Adrenergic sensitivity is present in impaired DRG neurons in the DRG chronic compression model; α1 and α2 adrenergic receptors are involved in excitatory adrenergic sensitivity; this adrenergic sensitivity is independent of Sympathetic postganglionic nerve endings.