糖尿病痛过敏大鼠尾神经中传入单位对交感传出的反应

Responses of afferent unit of the caudal nerve of diabetic hyperalgesic rats to sympathetic efferent stimulation

实验观察了刺激交感神经 (sympatheticstimulation ,SS)、静脉注射去甲肾上素 (noradrenaline ,NA)和酚妥拉明对糖尿病痛过敏大鼠尾神经中各种传入单位的影响。结果发现 ,糖尿病痛过敏大鼠的具有自发放电的C单位和Aδ单位在SS后放电频率增加 ,α 受体阻断剂能消除这些自发放电活动 ;在无自发放电的C单位和Aδ单位中 ,SS能使部分C单位和Aδ单位由静息状态转入活动状态 ;它虽不能诱发C 机械感受单位 (Cmechanicalreceptiveunit,C M)产生传入放电 ,但可诱发部分C 机械热单位 (Cmechano heatunit,C MH)和C 多型单位 (Cpolymodalunit,C Pol)的活动 ;SS还能使部分Aδ 机械单位 (Aδmechanicalreceptiveunit,Aδ M)和Aδ 机械热单位 (Aδmechano heatu nit,Aδ MH)产生传入放电 ;它所诱发的C单位和Aδ单位反应的潜伏期不等 ,但不短于 5s ;SS不能引起糖尿病痛过敏大鼠Aβ机械感受性单位和对照组大鼠各类感受性单位产生新的传入活动。静脉注射NA可诱发糖尿病痛过敏大鼠的部分C单位和Aδ单位产生新的传入活动。结果提示 。

Responses of afferent unit to sympathetic stimulation (SS), intravenous injection of noradrenaline (NA) and phentolamine in the caudal nerve of diabetic rats were investigated. The results showed that the discharge frequencies of C and Aδ units with spontaneous discharges were increased in diabetic hyperalgesic rats after SS, and these spontaneous discharges were eliminated by adrenergic antagonist. The C (6/21) and Aδ (19/81) units with no spontaneous discharges of diabetic hyperalgesic rat turned from silent state into active state during SS; although SS did not elicit afferent discharges of the C mechanical receptive units (C-M), it elicited afferent discharges of a part of C mechano-heat units (C-MH) and C polymodal units (C-Pol); afferent discharges of some of the Aδ mechanical receptive units (Aδ-M) and Aδ mechano-heat units (Aδ-MH) were also elicited by SS. The latencies of the C and Aδ units responses upon SS were not equal, but no less than 5 s. SS elicited neither afferent discharges from Aβ mechanical receptive units of diabetic hyperalgesic rat, nor receptive units of all types in the control rat. The C(3/8) and Aδ (4/12) units of diabetic hyperalgesic rat were activated by intravenous injection of NA. The present data suggest that NA released from sympathetic nerve terminals excites C and Aδ units of diabetic hypesthesic rat, which may be a peripheral factor in hyperalgesia and paresthesia of diabetic rats.