Skilling S R, Harkness D H, Larson A A
Department of Veterinary PathoBiology, University of Minnesota, St. Paul 55108.
Neurosci Lett. 1992 May 11;139(1):92-6. doi: 10.1016/0304-3940(92)90865-5.
Partial ligation of the sciatic nerve of rats produces hyperalgesia similar to that seen in humans following nerve injury. In this study, we used microdialysis of the spinal cord cerebral spinal fluid (CSF) to test the hypothesis that hyperalgesia is due to an enhanced release of excitatory amino acids (EAA) in response to substance P (SP). Intrathecal SP caused release of aspartate and glutamate in the CSF of rats with partial sciatic ligation at a dose of SP that did not cause release in sham operated animals. Neonatal capsaicin pretreatment blocked SP-induced EAA release in both sham and sciatic ligated animals. Release of EAAs in ligated animals was not significantly different from release in sham-operated animals following higher doses of SP or chemical nociceptive stimulation. These results demonstrate a partial sciatic ligation-induced decrease in the dose of SP required to initiate EAA release in the CSF of the spinal cord, a change which could play an important role in hyperalgesia.
大鼠坐骨神经部分结扎会产生类似于人类神经损伤后出现的痛觉过敏。在本研究中，我们采用脊髓脑脊液微透析技术来检验以下假设：痛觉过敏是由于对P物质（SP）产生反应时兴奋性氨基酸（EAA）释放增强所致。鞘内注射SP会导致部分坐骨神经结扎大鼠的脑脊液中天冬氨酸和谷氨酸释放，而该剂量的SP在假手术动物中不会引起释放。新生大鼠辣椒素预处理可阻断假手术和坐骨神经结扎动物中SP诱导的EAA释放。在更高剂量的SP或化学性伤害性刺激后，结扎动物中EAA的释放与假手术动物中的释放无显著差异。这些结果表明，坐骨神经部分结扎会导致脊髓脑脊液中启动EAA释放所需的SP剂量降低，这一变化可能在痛觉过敏中起重要作用。
