Seltzer Z, Shir Y
Physiology Branch, Faculty of Dental Medicine, Hebrew University of Jerusalem, Israel.
J Basic Clin Physiol Pharmacol. 1991 Jan-Jun;2(1-2):17-61. doi: 10.1515/jbcpp.1991.2.1-2.17.
Partial nerve injury is the main cause of sympathetically maintained causalgiform pain disorders in humans. We present here an animal model of this condition, produced in rats by a unilateral ligation of about half of the sciatic nerve. Starting hours after the operation and for several months thereafter, the rats developed signs of spontaneous pain, touch-evoked allodynia and hyperesthesia, and mechanical and thermal hyperalgesia in the partially denervated as well as the intact contralateral foot. These disorders were maintained by the sympathetic outflow and disappeared following postoperative sympathectomy. In neonatally capsaicinated rats we found that touch-evoked allodynia and hyperesthesia were mediated by A-fibers whereas thermal hyperalgesia was mediated by C-fibers. These disorders were not due to receptor sensitization of remaining afferent fibers by prostaglandins. We found strain differences and genetic inheritance of these causalgiform disorders which were correlated with the expression of autotomy to hind-paw denervation.
部分神经损伤是人类交感神经维持性灼痛样疼痛障碍的主要原因。我们在此展示一种该病症的动物模型，通过对大鼠坐骨神经约一半进行单侧结扎来制备。在手术后数小时开始，此后数月，大鼠在部分去神经支配的以及完整的对侧足部出现自发痛、触觉诱发的异常性疼痛和感觉过敏，以及机械性和热性痛觉过敏的迹象。这些障碍由交感神经传出活动维持，术后交感神经切除后消失。在新生期用辣椒素处理的大鼠中，我们发现触觉诱发的异常性疼痛和感觉过敏由A纤维介导，而热性痛觉过敏由C纤维介导。这些障碍并非由于前列腺素对剩余传入纤维的受体致敏所致。我们发现这些灼痛样障碍存在品系差异和遗传遗传性，且与后爪去神经支配后的自残行为表达相关。
