Affordable Access

Regional deafferentation down-regulates subtypes of glutamate transporter proteins.

Authors
  • Ginsberg, S D1
  • Martin, L J
  • Rothstein, J D
  • 1 Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Type
Published Article
Journal
Journal of Neurochemistry
Publisher
Wiley
Publication Date
Dec 01, 1995
Volume
65
Issue
6
Pages
2800–2803
Identifiers
PMID: 7595581
Source
Medline
License
Unknown

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.

Report this publication

Statistics

Seen <100 times