NDLI: Neuronal Expression of Splice Variants of “Glial” Glutamate Transporters in Brains Afflicted by Alzheimer’s Disease: Unmasking an Intrinsic Neuronal Property

Content Provider	Springer Nature Link
Author	Pow, David V. Cook, David G.
Copyright Year	2009
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.
Starting Page	1748
Ending Page	1757
Page Count	10
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	34
Issue Number	10
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2009-03-25
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Glutamate transporter Neurodegeneration Excitotoxicity GLT-1 GLAST EAAC1 Dementia Neurology Biochemistry Neurosciences
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Posttraumatic Epilepsy: Hemorrhage, Free Radicals and the Molecular Regulation of Glutamate

Expression of Glutamate Transporters EAAC1, GLAST, GLT-1 in Neonatal White Matter Play a Role in Brain Excitotoxicity

Glycolysis Inhibition Decreases the Levels of Glutamate Transporters and Enhances Glutamate Neurotoxicity in the R6/2 Huntington′s Disease Mice

Transient Focal Cerebral Ischemia Down-Regulates Glutamate Transporters GLT-1 and EAAC1 Expression in Rat Brain

Effects of Administered Ethanol and Methamphetamine on Glial Glutamate Transporters in Rat Striatum and Hippocampus

Calpains and Delayed Calcium Deregulation in Excitotoxicity

Distribution of Glutamate Transporter GLAST in Membranes of Cultured Astrocytes in the Presence of Glutamate Transport Substrates and ATP

Oncostatin M promotes excitotoxicity by inhibiting glutamate uptake in astrocytes: implications in HIV-associated neurotoxicity

Glutamate Differently Modulates Metabotropic Glutamate Receptors in Neuronal and Glial Cells

Neuronal Expression of Splice Variants of “Glial” Glutamate Transporters in Brains Afflicted by Alzheimer’s Disease: Unmasking an Intrinsic Neuronal Property

Similar Documents

Posttraumatic Epilepsy: Hemorrhage, Free Radicals and the Molecular Regulation of Glutamate

Expression of Glutamate Transporters EAAC1, GLAST, GLT-1 in Neonatal White Matter Play a Role in Brain Excitotoxicity

Glycolysis Inhibition Decreases the Levels of Glutamate Transporters and Enhances Glutamate Neurotoxicity in the R6/2 Huntington′s Disease Mice

Transient Focal Cerebral Ischemia Down-Regulates Glutamate Transporters GLT-1 and EAAC1 Expression in Rat Brain

Effects of Administered Ethanol and Methamphetamine on Glial Glutamate Transporters in Rat Striatum and Hippocampus

Calpains and Delayed Calcium Deregulation in Excitotoxicity

Distribution of Glutamate Transporter GLAST in Membranes of Cultured Astrocytes in the Presence of Glutamate Transport Substrates and ATP

Oncostatin M promotes excitotoxicity by inhibiting glutamate uptake in astrocytes: implications in HIV-associated neurotoxicity

Glutamate Differently Modulates Metabotropic Glutamate Receptors in Neuronal and Glial Cells

Neuronal Expression of Splice Variants of “Glial” Glutamate Transporters in Brains Afflicted by Alzheimer’s Disease: Unmasking an Intrinsic Neuronal Property