Mills C D, Xu G Y, Johnson K M, McAdoo D J, Hulsebosch C E
The Department of Anatomy and Neurosciences, The University of Texas Medical Branch at Galveston, 77555-1069, USA.
Neuroreport. 2000 Sep 28;11(14):3067-70. doi: 10.1097/00001756-200009280-00007.
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.
脊髓损伤（SCI）会导致细胞外兴奋性氨基酸（EAA）浓度升高，从而引发谷氨酸受体介导的兴奋性毒性和中枢敏化。为了测试I组代谢型谷氨酸受体（mGluRs）在脊髓损伤诱导的谷氨酸释放以及损伤后中枢敏化行为结果中的作用，我们在脊髓挫伤损伤后立即给大鼠鞘内注射1-氨基茚满-1,5-二羧酸（AIDA；0.1 nmol），一种有效的I组mGluR拮抗剂。通过微透析收集EAA，并使用高效液相色谱法进行定量。AIDA显著降低了细胞外谷氨酸浓度，但对天冬氨酸浓度无影响，并且显著减轻了机械性异常性疼痛的发展，但对热痛觉过敏无影响。这些结果表明，mGluRs在脊髓损伤诱导的EAA释放和中枢敏化中起重要作用。
