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Glutamate transporter EAAC1 is expressed in neurons and glial cells in the rat nervous system
Author(s) -
Kugler Peter,
Schmitt Angelika
Publication year - 1999
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/(sici)1098-1136(199908)27:2<129::aid-glia3>3.0.co;2-y
Subject(s) - biology , immunolabeling , neuroglia , central nervous system , immunocytochemistry , ependymal cell , in situ hybridization , oligodendrocyte , glutamate aspartate transporter , microbiology and biotechnology , glutamate receptor , myelin , neuroscience , immunohistochemistry , messenger rna , endocrinology , biochemistry , immunology , metabotropic glutamate receptor , receptor , gene
Oligonucleotide and cRNA probes were used for non‐radioactive in situ hybridization, carried out to identify the cell types in the nervous system of rat expressing the glutamate transporter EAAC1 mRNA. The results were compared with immunocytochemical data obtained using an antibody against a synthetic EAAC1 peptide. The present data confirm that EAAC1 is expressed in neurons of the CNS. Additionally, our findings indicate the localization of EAAC1 mRNA and protein in peripheral neurons (spinal ganglia) and in glial cells, i.e., oligodendrocytes in various white matter regions of the CNS, ependymal cells, and epithelial cells of the plexus choroideus of the four ventricles, as well as in satellite cells of spinal ganglia. Immunolabeling revealed a preferentially cytoplasmic staining of neurons and glial cells. The cytoplasmic staining was frequently granular, suggesting a localization of EAAC1 protein in vesicle membranes. A membrane localization of EAAC1 was also indicated by Western blotting, which showed immunoreactivity only in the 100,000 × g pellet of brain homogenate. We conclude that the glutamate transporter EAAC1 is not restricted to neurons but may also play an important role in glial cells, particularly in oligodendrocytes. GLIA 27:129–142, 1999. © 1999 Wiley‐Liss, Inc.