Neuronal expression of splice variants of "Glial" glutamate transporters in brains afflicted by alzheimer's disease: unmasking an intrinsic neuronal property

Pow, David V. and Cook, David G. (2009) Neuronal expression of splice variants of "Glial" glutamate transporters in brains afflicted by alzheimer's disease: unmasking an intrinsic neuronal property. Neurochemical Research, 34 10: 1748-1757. doi:10.1007/s11064-009-9957-0


Author Pow, David V.
Cook, David G.
Title Neuronal expression of splice variants of "Glial" glutamate transporters in brains afflicted by alzheimer's disease: unmasking an intrinsic neuronal property
Journal name Neurochemical Research   Check publisher's open access policy
ISSN 0364-3190
Publication date 2009-10-01
Year available 2009
Sub-type Article (original research)
DOI 10.1007/s11064-009-9957-0
Open Access Status Not yet assessed
Volume 34
Issue 10
Start page 1748
End page 1757
Total pages 10
Editor Abel Lajtha
Place of publication New York, N.Y, United States
Publisher Springer New York LLC
Language eng
Subject 110902 Cellular Nervous System
C1
920112 Neurodegenerative Disorders Related to Ageing
Abstract Anomalies in glutamate homeostasis may contribute to the pathological processes involved in Alzheimer's disease (AD). Glutamate released from neurons or glial cells is normally rapidly cleared by glutamate transporters, most of which are expressed at the protein level by glial cells. However, in some patho-physiological situations, expression of glutamate transporters that are normally considered to be glial types, appears to be evoked in populations of distressed neurons. This study analysed the expression of exon-skipping forms of the three predominant excitatory amino acid (glutamate) transporters (EAATs1-3) in brains afflicted with AD. We demonstrate by immunocytochemistry in temporal cortex, the expression of these proteins particularly in limited subsets of neurons, some of which appeared to be dys-morphic. Whilst the neuronal expression of the "glial" glutamate transporters EAAT1 and EAAT2 is frequently considered to represent the abnormal and ectopic expression of such transporters, we suggest this may be a misinterpretation, since neurons such as cortical pyramidal cells normally express abundant mRNA for these EAATs (but little if any EAAT protein expression). We hypothesize instead that distressed neurons in the AD brain can turn on the translation of pre-existent mRNA pools, or suppress the degradation of alternately spliced glutamate transporter protein, leading to the "unmasking" of, rather than evoked expression of "glial" glutamate transporters in stressed neurons.
Keyword Glutamate transporter
Neurodegeneration
Excitotoxicity
Glt-1
Glast
EAAC1
dementia
Alzheimer's Disease
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: UQ Centre for Clinical Research Publications
2010 Higher Education Research Data Collection
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 10 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 11 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Thu, 03 Sep 2009, 17:41:27 EST by Mr Andrew Martlew on behalf of UQ Centre for Clinical Research