Sheen K, Chung J M
Marine Biomedical Institute, University of Texas Medical Branch, Galveston 77555-0843.
Brain Res. 1993 Apr 30;610(1):62-8. doi: 10.1016/0006-8993(93)91217-g.
The present study was undertaken to determine the role of injured fibers in the development of neuropathic pain using our earlier established rat model. Our model was produced by placing tight ligatures to the L5 or both the L5 and L6 spinal nerves on one side in the rat. These rats showed long-lasting behavioral signs of mechanical allodynia and heat hyperalgesia. Using the uniqueness of our model, 3 specific questions are being asked concerning the initiation and maintenance of behavioral signs for neuropathic pain. The results of behavioral tests performed after various surgical manipulations suggest that: (1) peripheral nerve injury itself is the critical factor for the development of behavioral signs of neuropathic pain; (2) signs of neuropathic pain appear only when injury occurs at a part of the peripheral nerve distal to the dorsal root ganglion; and (3) signals (either electrical or chemical) entering the spinal cord from the injured fibers or the dorsal root ganglion cells play a critical role for both initiation and maintenance of the neuropathic pain state.
本研究旨在利用我们早期建立的大鼠模型,确定受损纤维在神经性疼痛发展中的作用。我们的模型是通过在大鼠一侧对L5或L5和L6脊髓神经进行紧密结扎而建立的。这些大鼠表现出机械性异常性疼痛和热痛觉过敏的长期行为体征。利用我们模型的独特性,针对神经性疼痛行为体征的起始和维持提出了3个具体问题。各种手术操作后进行的行为测试结果表明:(1) 周围神经损伤本身是神经性疼痛行为体征发展的关键因素;(2) 仅当损伤发生在背根神经节远端的周围神经部分时,才会出现神经性疼痛体征;(3) 从受损纤维或背根神经节细胞进入脊髓的信号(电信号或化学信号)对神经性疼痛状态的起始和维持都起着关键作用。