Expression of the exon 9-skipping form of EAAT2 in astrocytes of rats

Macnab, L.T. and Pow, D.V. (2007) Expression of the exon 9-skipping form of EAAT2 in astrocytes of rats. Neuroscience, 150 3: 705-711. doi:10.1016/j.neuroscience.2007.09.049


Author Macnab, L.T.
Pow, D.V.
Title Expression of the exon 9-skipping form of EAAT2 in astrocytes of rats
Journal name Neuroscience   Check publisher's open access policy
ISSN 0306-4522
1873-7544
0361-0713
Publication date 2007-12-12
Sub-type Article (original research)
DOI 10.1016/j.neuroscience.2007.09.049
Volume 150
Issue 3
Start page 705
End page 711
Total pages 7
Editor O. P. Ottersen
Place of publication Oxford, U.K.
Publisher Pergamon
Language eng
Subject 1109 Neurosciences
Formatted abstract
mRNA for the exon 9-skipping form of the glutamate transporter excitatory amino acid transporter (EAAT) 2 (glutamate transporter 1, GLT-1) is known to be expressed in brain and spinal cord, and such expression was initially proposed to be associated with motor neuron disease. Surprisingly, a protein corresponding to the size of this splice variant has not previously been detected when using antibodies against one of the possible carboxyl terminal regions of EAAT2. This has been construed as indicating that little of the exon 9-skipping protein is expressed, or that such protein is not stable. We have now made selective antibodies against the splice site of this form of EAAT2. We show that in the adult rat brain and spinal cord, it is expressed primarily in populations of white matter astrocytes. Astrocytes expressing this splice variant also expressed glial fibrillary acidic protein. Expression was developmentally regulated, being expressed in a small number of astrocytes at postnatal day 7, but strongly expressed by large populations of white matter astrocytes by 25 days postnatum and into adulthood. Only a subset of gray matter astrocytes and radial glia expressed exon 9-skipping EAAT2. We suggest that exon 9-skipping EAAT2 may have a role in regulating extracellular glutamate in white matter tracts, either by interacting with normally spliced EAAT2 and modifying its targeting or transport activity, or by acting as a transporter itself. Conversely, the limited expression in gray matter suggests it is unlikely to be important for modulating synaptic levels of glutamate.
© 2007 IBRO.
Keyword Astrocytes
Western blotting
Cerebellum
Corpus callosum
Excitatory amino acid transporter 2
Exons
Glutamic acid
Hippocampus
Immunoblotting
Immunohistochemistry
Nerve fibers, myelinated
Rats, inbred strains
RNA splicing
Q-Index Code C1

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
School of Biomedical Sciences Publications
 
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