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

Spinal cord injury (SCI) leads to an increase in extracellular excitatory a mino acid (EAA) concentrations, resulting in glutamate receptor-mediated ex citotoxicity and central sensitization. To test contributions of group I me tabotropic glutamate receptors (mGluRs) in SCI induced release of glutamate and in behavioral outcomes of central sensitization following injury, we a dministered 1-aminoindan-1,5-dicarboxylic acid (AIDA; 0.1 nmol intraspinall y), a potent group I mGluR antagonist, to rats immediately after spinal cor d contusion injury. EAAs were collected by microdialysis and quantified usi ng HPLC. AIDA significantly decreased extracellular glutamate but not aspar tate concentrations and significantly attenuated the development of mechani cal but not thermal allodynia. These results suggest mGluRs play an importa nt role in injury-induced EAA release and in central sensitization followin g SCI. NeuroReport 11:3067-3070 (C) 2000 Lippincott Williams & Wilkins.