Urban L, Thompson S W, Dray A
Dept of Pharmacology, Sandoz Institute for Medical Research, London, UK.
Trends Neurosci. 1994 Oct;17(10):432-8. doi: 10.1016/0166-2236(94)90018-3.
Activation of C fibres with strong 'potentially tissue damaging' chemical, mechanical or thermal stimuli produces painful sensations that are significantly enhanced during pathological conditions, such as neuropathy and inflammation. The pronounced painful symptoms of hyperalgesia and allodynia are induced, in part, by the development of spinal hyperexcitability. This involves plastic changes in synaptic transmission between primary afferents and dorsal horn neurones induced by sustained activity of peripheral nociceptors. L. Urban, S. W. N. Thompson and A. Dray describe some of the central mechanisms that account for central hyperexcitability occurring in hyperalgesia and allodynia based on evidence from experiments both in vivo and in vitro with neurokinin and N-methyl-D-aspartate receptor antagonists.
用强烈的“潜在组织损伤性”化学、机械或热刺激激活C纤维会产生疼痛感，在诸如神经病变和炎症等病理状态下，这种疼痛感会显著增强。痛觉过敏和异常性疼痛的明显疼痛症状部分是由脊髓兴奋性过高引起的。这涉及到外周伤害感受器持续活动诱导的初级传入神经和背角神经元之间突触传递的可塑性变化。L. 厄本、S. W. N. 汤普森和A. 德雷根据体内和体外实验中使用神经激肽和N-甲基-D-天冬氨酸受体拮抗剂的证据，描述了一些导致痛觉过敏和异常性疼痛中出现中枢兴奋性过高的中枢机制。
