Garrison C J, Dougherty P M, Carlton S M
Department of Anatomy and Neuroscience, University of Texas Medical Branch, Galveston 77555-0843.
Exp Neurol. 1994 Oct;129(2):237-43. doi: 10.1006/exnr.1994.1165.
The objective of the present investigation was to determine if baseline glial fibrillary acidic protein (GFAP) expression and the increases in GFAP expression induced by chronic constriction of the sciatic nerve were modified by the specific N-methyl-D-aspartate (NMDA) receptor antagonist MK-801. Changes in immunohistochemical staining densities of GFAP within the L4 spinal cord were quantified and compared in three groups of animals: (1) nonneuropathic rats, (2) nondrug-treated neuropathic rats, and (3) neuropathic rats treated for 7 days with MK-801. The results indicate that baseline GFAP staining density in naive animals is dependent on NMDA receptor activity and that an ongoing NMDA-dependent signal is, at least in part, responsible for the increase in GFAP observed following peripheral nerve injury.
本研究的目的是确定特定的N-甲基-D-天冬氨酸（NMDA）受体拮抗剂MK-801是否会改变基线胶质纤维酸性蛋白（GFAP）的表达以及坐骨神经慢性压迫诱导的GFAP表达增加。对三组动物L4脊髓内GFAP免疫组化染色密度的变化进行了量化和比较：（1）非神经性大鼠，（2）未接受药物治疗的神经性大鼠，以及（3）用MK-801治疗7天的神经性大鼠。结果表明，未处理动物的基线GFAP染色密度依赖于NMDA受体活性，并且持续的NMDA依赖性信号至少部分地导致了外周神经损伤后观察到的GFAP增加。
