An adenoviral vector expressing the glucose transporter protects cultured striatal neurons from 3-nitropropionic acid

Considerable interest has focused on the possibility of using gene transfer techniques to introduce protective genes into neurons around the time of necrotic insults. We have previously used herpes simplex virus amplicon vectors to overexpress the rat brain glucose transporter, Glut-1 (GT), and have...

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Bibliographic Details
Published in:Brain research 2000-03, Vol.859 (1), p.21-25
Main Authors: Fink, Sheri L., Ho, Dora Y., McLaughlin, John, Sapolsky, Robert M.
Format: Article
Language:English
Subjects:
3-Nitropropionic acid
Adenoviridae
Adenovirus
Animals
Biological and medical sciences
Biotechnology
Cell Culture Techniques
Convulsants - toxicity
Corpus Striatum - cytology
Corpus Striatum - drug effects
Corpus Striatum - metabolism
Fetus
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Viral
Gene therapy
Genetic Vectors
Glucose transport
glucose transporter
Glucose Transporter Type 1
Health. Pharmaceutical industry
Industrial applications and implications. Economical aspects
Monosaccharide Transport Proteins - genetics
Monosaccharide Transport Proteins - metabolism
Neuron death
Neuronal energetics
Neurons - drug effects
Neurons - metabolism
Neurons - virology
Neuroprotective Agents - metabolism
Nitro Compounds
Propionates - toxicity
Rats
Rats, Sprague-Dawley
Striatum
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Summary:Considerable interest has focused on the possibility of using gene transfer techniques to introduce protective genes into neurons around the time of necrotic insults. We have previously used herpes simplex virus amplicon vectors to overexpress the rat brain glucose transporter, Glut-1 (GT), and have shown it to protect against a variety of necrotic insults both in vitro and in vivo, as well as to buffer neurons from the steps thought to mediate necrotic injury. It is critical to show the specificity of the effects of any such transgene overexpression, in order to show that protection arises from the transgene delivered, rather than from the vector delivery system itself. As such, we tested the protective potential of GT overexpression driven, in this case, by an adenoviral vector, against a novel insult, namely exposure of primary striatal cultures to the metabolic poison, 3-nitropropionic acid (3NP). We observed that GT overexpression buffered neurons from neurotoxicity induced by 3NP.
ISSN:0006-8993
1872-6240
DOI:10.1016/S0006-8993(99)02401-4