Saadé Nayef E, Al Amin Hassen, Chalouhi Steven, Baki Samah Abdel, Jabbur Suhayl J, Atweh Samir F
Department of Human Morphology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Pain. 2006 Dec 15;126(1-3):280-93. doi: 10.1016/j.pain.2006.07.010. Epub 2006 Aug 30.
Controversial results have been recently reported on the role of supraspinal centers in the modulation of nociceptive behavior in animal models of mononeuropathy. Our aim was to investigate the role of the various spinal pathways in the modulation of the neuropathic manifestations. Several groups of rats were subjected to selective spinal-tract lesions, either 2-3 weeks before or 2-3 weeks after the induction of mononeuropathy following the chronic constriction injury (CCI) or the spared nerve injury (SNI) models. Tactile and cold allodynias were assessed by Von Frey filaments and the acetone drops test, respectively. Thermal hyperalgesia was assessed by the paw withdrawal and the hot plate tests. The effects of unilateral and bilateral lesions of the dorso-lateral funiculus (DLF), the anterolateral column (ALC) or hemisection were tested over a period of 4-8 weeks. All spinal tract lesions produced reversible, but significant decrease of allodynia and hyperalgesia over a period of 1-3 weeks. The most pronounced effects were observed with bilateral lesions. The stronger attenuation was observed on thermal hyperalgesia, assessed by the paw withdrawal test, while cold allodynia was the least affected. Spinal lesions performed before the induction of neuropathy did not produce significant alterations in the temporal development of neuropathic manifestations. The present results allow the conclusion that all spinal tracts can be involved in the rostral transmission and the descending modulation of neuropathic manifestations. The recovery of symptoms following spinal lesions provides illustration on the plasticity of the neural network involved in the processing of the neuropathic syndromes.
最近有关于脊髓上中枢在单神经病动物模型中对伤害性感受行为调节作用的争议性结果报道。我们的目的是研究各种脊髓通路在神经病理性表现调节中的作用。几组大鼠在慢性压迫损伤（CCI）或保留神经损伤（SNI）模型诱导单神经病之前或之后2 - 3周接受选择性脊髓束损伤。分别通过von Frey细丝和丙酮滴试验评估触觉性和冷觉异常性疼痛。通过足趾退缩和热板试验评估热痛觉过敏。在4 - 8周的时间内测试背外侧索（DLF）、前外侧柱（ALC）单侧和双侧损伤或半横断的效果。所有脊髓束损伤在1 - 3周内均产生可逆但显著的异常性疼痛和痛觉过敏减轻。双侧损伤观察到最明显的效果。通过足趾退缩试验评估，热痛觉过敏的减弱更强，而冷觉异常性疼痛受影响最小。在诱导神经病变之前进行的脊髓损伤在神经病理性表现的时间发展上未产生显著改变。目前的结果可以得出结论，所有脊髓束都可能参与神经病理性表现的向头端传递和下行调节。脊髓损伤后症状的恢复说明了参与神经病理性综合征处理的神经网络的可塑性。
