Wakisaka S, Kajander K C, Bennett G J
Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892.
Brain Res. 1992 Dec 11;598(1-2):349-52. doi: 10.1016/0006-8993(92)90206-o.
Changes in neuropeptide Y-like immunoreactivity (NPYir) in the rat L4 and L5 spinal cord and dorsal root ganglia (DRG) were examined after different sciatic nerve injuries (transection, loose ligation, and crush) and a localized, painful inflammation of the hind paw. Inflammation had no effect on NPYir. All the nerve injuries produced comparable increases in NPYir in ipsilateral laminae III-V axons and varicosities, and induction of NPYir in many DRG cells. Most NPYir DRG cells were medium to large (mean diameters: 40-45 microns); less than 2% of the cells had diameters of 25 microns or less. We conclude that the nerve injury-evoked increase in NPYir occurs mostly in the somata and intraspinal arbors of low-threshold mechanoreceptors; very few, if any, C-fiber afferents are involved. Nerve injury, rather than a painful condition, appears to be the stimulus for the induction of NPYir synthesis.
在大鼠坐骨神经遭受不同损伤(横断、松结扎和挤压)以及后爪局部疼痛性炎症后,检测了大鼠L4和L5脊髓及背根神经节(DRG)中神经肽Y样免疫反应性(NPYir)的变化。炎症对NPYir无影响。所有神经损伤均使同侧III - V层轴突和膨体中的NPYir出现类似程度的增加,并在许多DRG细胞中诱导NPYir表达。大多数表达NPYir的DRG细胞为中等至大型(平均直径:40 - 45微米);直径为25微米或更小的细胞不到2%。我们得出结论,神经损伤诱发的NPYir增加主要发生在低阈值机械感受器的胞体和脊髓内分支中;极少有C纤维传入纤维(若有的话)参与其中。神经损伤而非疼痛状态似乎是诱导NPYir合成的刺激因素。