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

反射性交感神经营养不良疼痛诱发机制的实验研究

基本信息

批准号：
04454385
负责人：
SHIMOJI Koki
金额：
$ 3.78万
依托单位：
NIIGATA UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1992
资助国家：
日本
起止时间：
1992 至 1993
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-04454385/
关键词：
Refractory sensory nerve dystrophy Sciatic nerve Intracellular recording Substantia gelatinosa neuron Spinal cord potential Supraspinal structures 坐骨神経神経破壊

项目摘要

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.

为探讨反射性交感神经营养不良（RSD）痛诱发机制，观察了RSD模型大鼠的行为学变化，并记录了其脊髓神经元在体和离体的活动。采用机械或化学方法损毁大鼠坐骨神经，制备RSD模型。坐骨神经破坏后，观察到异常行为，如咬后爪，跑步运动和截瘫。假手术组动物未出现异常行为。在正常成年大鼠脑片的细胞内记录中，在对背根刺激作出反应的胶状质神经元中，发现了仅由Asigma和C纤维介导的单突触EPSP和IPSP，而不由A α/β纤维介导。在少数胶状质神经元中记录到由A α/β纤维激活的多突触后电位。在RSD模型大鼠中，在大多数胶状质神经元中观察到激活asigma和C纤维的单突触电位和通过A α/β纤维的多突触输入。在RSD模型大鼠的脑片制备中，在背根刺激后也观察到胶状质神经元的重复放电。在正常大鼠L4/5记录到由两个正电位（HSP 1、HSP 2）和负电位组成的异节段脊髓电位。在RSD模型动物中，观察到HSP 1和HSP 2的峰值振幅显著增强和持续时间延长。由于这些电位可能是通过脊髓上结构的反馈回路产生的，因此认为在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是由节段性和脊髓上结构介导的。