脊髓挫伤损伤后兴奋性毒素喹啉酸水平升高。

Increased levels of the excitotoxin quinolinic acid in spinal cord following contusion injury.

作者信息

Blight A R, Saito K, Heyes M P

机构信息

Division of Neurosurgery, University of North Carolina at Chapel Hill 27599-7060.

出版信息

Brain Res. 1993 Dec 31;632(1-2):314-6. doi: 10.1016/0006-8993(93)91167-q.

DOI:10.1016/0006-8993(93)91167-q

PMID:8149236

Abstract

Products of inflammatory phagocytes are potential contributors to secondary pathology following spinal cord trauma. In the present study we quantified the levels of the neurotoxin and product of activated macrophages, quinolinic acid (QUIN), in the lower thoracic spinal cord of adult guinea pigs 5 days after brief compression injury. At the injured site (T13), elevations in tissue QUIN levels (> 10-fold) accompanied proportional increases in the activity of indoleamine-2,3 dioxygenase (> 2-fold) and the concentrations of L-kynurenine (> 2.5-fold). In contrast, no significant changes occurred in two uninjured regions examined compared to controls, namely cervical spinal cord (C2) and the somatosensory cortex. Further studies of QUIN as a potential contributor to spinal cord injury are warranted.

摘要

炎症吞噬细胞的产物是脊髓损伤后继发性病理变化的潜在促成因素。在本研究中，我们对成年豚鼠短暂压迫性损伤5天后下胸段脊髓中神经毒素和活化巨噬细胞产物喹啉酸（QUIN）的水平进行了定量。在损伤部位（T13），组织QUIN水平升高（>10倍），同时吲哚胺-2,3双加氧酶活性成比例增加（>2倍），L-犬尿氨酸浓度增加（>2.5倍）。相比之下，与对照组相比，所检查的两个未损伤区域，即颈脊髓（C2）和体感皮层，没有发生显著变化。有必要对QUIN作为脊髓损伤潜在促成因素进行进一步研究。