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疼痛性神经病变模型及神经挤压模型中脊髓背角的神经递质

Neurotransmitters in the spinal cord dorsal horn in a model of painful neuropathy and in nerve crush.

作者信息

Sommer C, Myers R R

机构信息

Department of Anesthesiology, University of California, San Diego, USA.

出版信息

Acta Neuropathol. 1995;90(5):478-85. doi: 10.1007/BF00294809.

DOI:10.1007/BF00294809
PMID:8560981
Abstract

We tested the hypothesis that neurochemical changes in the spinal cord dorsal horn associated with neuropathic pain states differ from those seen in association with non-painful neuropathies. Immunohistochemistry was performed on spinal cord sections from rats with a chronic constriction injury (CCI), which develop hyperalgesia, and from animals with a nerve crush injury, which do not develop hyperalgesia or other signs of a painful syndrome. Immunohistochemistry was quantified by computer-assisted densitometry. Calcitonin gene-related peptide (CGRP) immunoreactivity and substance P (SP) immunoreactivity were decreased from 1 to 4 weeks after injury in CCI and from 2 to 6 weeks in crush. Gamma-aminobutyric acid immunoreactivity was unchanged in both conditions at all time points. Met-enkephalin (Met-enk) immunoreactivity was increased in CCI and unchanged in crush. Although SP and CGRP are involved in pain transmission, we conclude that their decrease in immunoreactivity is not specific for the CCI model, but rather a more general event in nerve de- and regeneration. The increase in immunoreactivity for the opioid peptide Met-ink, however, was only seen in the late phase of CCI, and may be specific for conditions associated with neuropathic pain and its resolution.

摘要

我们检验了这样一个假设

与神经性疼痛状态相关的脊髓背角神经化学变化不同于与非疼痛性神经病变相关的变化。对患有慢性压迫性损伤(CCI)并出现痛觉过敏的大鼠以及患有神经挤压伤但未出现痛觉过敏或其他疼痛综合征体征的动物的脊髓切片进行免疫组织化学检测。免疫组织化学通过计算机辅助密度测定法进行定量分析。降钙素基因相关肽(CGRP)免疫反应性和P物质(SP)免疫反应性在CCI损伤后1至4周以及挤压伤后2至6周降低。γ-氨基丁酸免疫反应性在两种情况下的所有时间点均未改变。甲硫氨酸脑啡肽(Met-enk)免疫反应性在CCI中增加,在挤压伤中未改变。尽管SP和CGRP参与疼痛传递,但我们得出结论,它们免疫反应性的降低并非CCI模型所特有,而是神经退变和再生过程中更普遍的现象。然而,阿片肽Met-ink免疫反应性的增加仅在CCI后期出现,可能是与神经性疼痛及其缓解相关情况所特有的。

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