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

为探讨反射性交感神经营养不良(RSD)的疼痛诱导机制，我们观察了RSD模型大鼠的行为，并记录了其在体内和体外脊髓的神经元活动。RSD模型大鼠为PREPA，因机械或化学破坏坐骨神经而发红。坐骨神经损毁后，动物出现咬后爪、奔跑、截瘫等异常行为。未损毁坐骨神经的假手术组动物未见异常行为。在正常成年大鼠脑片上的细胞内记录中，仅由Asigma和C纤维介导的单突触EPSP和IPSP，而不是由Apha/β纤维介导的单突触的EPSP和IPSP，反应于背根刺激的胶状实质神经元。在少数胶状质神经元上记录到由Aα/β纤维激活的多突触后电位。在RSD模型大鼠的大部分胶状质神经元中，可观察到单突触电位激活的Asigma和C纤维，以及通过Apha/β纤维的多突触输入。在RSD模型大鼠的脑片制备中，还观察到背根刺激后胶状质神经元的重复放电。正常大鼠在L4/5处记录到由两个正电位(HSP1、HSP2)和前一个负电位组成的异位节段脊髓电位。在RSD模型动物中，HSP1和HSP2的峰值波幅和时程延长明显增强。由于这些电位可能是通过脊髓上结构的反馈环产生的，因此在RSD模型大鼠中观察到的神经元异常兴奋和抑制电位的增强被认为是由节段性结构和脊髓上结构共同介导的。

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.