Experimental study on the mechanism of pain induction in the reflex sympathetic dystrophy

为了探讨反射性交感神经营养不良（RSD）疼痛诱导的机制，我们在体内和体外观察了RSD模型大鼠的行为并记录了其脊髓神经元的活动。制备rsd模型大鼠；红色由机械或化学破坏坐骨神经。坐骨神经破坏后出现咬后爪、奔跑动作、截瘫等异常行为。假手术动物无坐骨神经损伤，未见异常行为。在正常成年大鼠的细胞内切片记录中，在对背根刺激反应的明胶质神经元中发现单突触EPSP和单突触EPSP仅由Asigma和C纤维介导，而不是由α / β纤维介导。在少数明胶质神经元中记录到由α / β纤维激活的突触后多电位。在RSD模型大鼠中，大多数明胶质神经元存在激活assigma和C纤维的单突触电位和通过α / β纤维的多突触输入。在RSD模型大鼠的切片制备中，在背根刺激后也观察到明胶质神经元的重复放电。正常大鼠L4/5脊髓异节段电位由HSP1、HSP2两个正电位组成，负电位先于正电位。在RSD模型动物中，HSP1和HSP2的峰值增强，持续时间延长。由于这些电位可能是通过棘上结构的反馈回路产生的，因此在RSD模型大鼠中观察到的异常神经元兴奋和抑制电位的增强被认为是由节段结构和棘上结构介导的。

To investigate the mechanism of pain induction in reflex sympathetic dystrophy (RSD), we observed behaviors of RSD model rats and recorded neuronal activities of their spinal cord in vivo and in vitro. The RSD-model rats were prepa ; red by mechanical or chemical destruction of the sciatic nerve. Following the sciatic nerve destruction, abnormal behaviors such as biting the hind paws, running motion and paraplegia were observed. No abnormal behavior were observed in sham operated animal without the sciatic nerve destruction. In intracellular recording in the slice preparations of normal adult rats, monosynapotic EPSP and IPSP mediated by only the Asigma and C fibers, not by the Aalpha/beta fibers, werefound in substanitia gelatinosa neurons in respose to dorsal root stimulation. Polysynaptic postsynapyic potentials activated by Aalpha/beta fibers were recorded in a few substantia gelatinosa neurons. In the RSD model rats, monosynaptic potentials activated asigma and C fibers and polysynaptic inputs viaAalpha/beta fibers were observed in a majority of substantia gelatinosa neurons. Repetitive firings in substantia gelatinosa neurons were also observed following a dorsal root stimulation in slice preparations of the RSD model rats. Hetero-segmental spinal cord potentials consisted of two positive potentials (HSP1, HSP2) preceded by negatibe potentials were recorded at L4/5 in normal rats. There observed significant intensification in peak amplitude and elongation in duration in HSP1 and HSP2 in the RSD model animals. As these potentials might be produced by a feedback loop via supraspinal structures, abnormal neuronal excitation and intensification of the inhibitory potentials observed in the RSD model rats were thought to be mediated by segmental as well as supraspinal structures.