AIDA reduces glutamate release and attenuates mechanical allodynia after spinal cord injury

被引：45

作者：

Mills, CD ^{[1
]}

Xu, GY ^{[1
]}

Johnson, KM ^{[1
]}

McAdoo, DJ ^{[1
]}

Hulsebosch, CE ^{[1
]}

机构：

[1] Univ Texas, Med Branch, Dept Anat & Neurosci, Galveston, TX 77555 USA

来源：

NEUROREPORT | 2000年 / 11卷 / 14期

关键词：

AIDA; metabotropic glutamate receptor; spinal cord injury;

D O I：

10.1097/00001756-200009280-00007

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Spinal cord injury (SCI) leads to an increase in extracellular excitatory amino acid (EAA) concentrations, resulting in glutamate receptor-mediated excitotoxicity and central sensitization. To test contributions of group I metabotropic glutamate receptors (mGluRs) in SCI induced release of glutamate and in behavioral outcomes of central sensitization following injury, we administered 1-aminoindan-1,5-dicarboxylic acid (AIDA; 0.1 nmol intraspinally), a potent group I mGluR antagonist, to rats immediately after spinal cord contusion injury. EAAs were collected by microdialysis and quantified using HPLC. AIDA significantly decreased extracellular glutamate but not aspartate concentrations and significantly attenuated the development of mechanical but not thermal allodynia. These results suggest mGluRs play an important role in injury-induced EAA release and in central sensitization following SCI. NeuroReport 11:3067-3070 (C) 2000 Lippincott Williams & Wilkins.

引用

页码：3067 / 3070

页数：4

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