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Regional Deafferentiation Down‐Regulates Subtypes of Glutamate Transporter Proteins

Abstract: Low extracellular glutamate content is maintained primarily by high‐affinity sodium‐dependent glutamate transport. Three glutamate transporter proteins have been cloned: GLT‐1 and GLAST are astroglial, whereas EAAC1 is neuronal. The effects of axotomy on glutamate transporter expression was evaluated in adult rats following unilateral fimbria‐fornix and corticostriatal lesions. The hippocampus and striatum were collected at 3, 7, 14, and 30 days postlesion. Homogenates were immunoblotted using antibodies directed against GLT‐1, GLAST, EAAC1, and glial fibrillary acidic protein and assayed for glutamate transport by d‐[3H]aspartate binding. GLT‐1 immunoreactivity was decreased within the ipsilateral hippocampus and striatum at 14 days postlesion. GLAST immunoreactivity was decreased within the ipsilateral hippocampus and striatum at 7 and 14 days postlesion. No alterations in EAAC1 immunoreactivity were observed. d‐[3H]Aspartate binding was decreased at 14 days postlesion within the ipsilateral hippocampus and at 7 and 14 days postlesion within the ipsilateral striatum. By 30 days postlesion, glutamate transporters and d‐[3H]aspartate binding returned to control levels. This study demonstrates the down‐regulation of primarily glial, and not neuronal, glutamate transporters following regional disconnection.