目的:研究利鲁唑(riluzole)对受损背根节(DRG)A类神经元的不同模式自发放电的作用,并探讨其可能机制。方法:本实验在大鼠L5椎间孔置入不锈钢柱制备大鼠DRG慢性压迫模型(chronic compression of DRG,CCD)上,利用在体单纤维记录的方法观察DRG局部浸浴利鲁唑(500μmol/L)对受损DRG神经元自发放电的影响。结果:(1)CCD大鼠手术后表现出明显的损伤侧机械刺激缩足阈值降低(P<0.05);(2)利鲁唑对受损DRG神经元自发放电具有明显抑制作用(n=30,P<0.05);(3)利鲁唑对非周期放电频率的抑制率显著大于对周期放电频率的抑制率(P<0.05)。结论:利鲁唑对慢性压迫DRGA类神经元的自发放电有显著抑制作用,对非周期放电的抑制作用明显大于对周期放电的作用,呈现出"非周期敏感"的特点,提示受损DRG神经元非周期自发放电行为处于更加不稳定的动力学状态。
Animals and humans share similar mechanisms of pain detection and similar brain areas involved in pain processing.Also,they show similar pain behaviors,such as reflexed sensation to nociceptive stimuli.Pain is often described in sensory discrimination （algosity） and affective motivation （unpleasantness） dimensions.Both basic and clinical findings indicate that individuals with chronic pain usually suffer more from pain-associated affective disturbances than from the actual pain sensations per se.Although the neural systems responsible for the sensory component of pain have been studied extensively,the neural mechanisms underlying negative affective component are not well understood.This is partly due to the relative paucity of animal paradigms for reliable examination of each component of pain.In humans,the experience of pain and suffering can be reported by language,while in animals,pain can only be inferred through physical and behavioral reactions.Animal behaviors,cognitive psychology and functional brain imaging have made it possible to assess pain affection and pain memory in animals.Animals subjected to either neuropathic injury or inflammatory insult display significant conditioned place aversion to a pain-paired environment in behaviors.The present review aims to summarize the common methods of affective unpleasantness assessment in rats.
