Modulation of Tau Neuronal Expression Induced by NMDA, non-NMDA and Metabotropic Glutamate Receptor Agonists

We have analysed changes in tau protein immunoreactivity in rat embryonic neurons degenerating in response to treatment with N-methyl-D-aspartate (NMDA), non-NMDA and metabotropic agonists. Glutamate agonists were applied in a Mg++-free and glycine-supplemented medium 8 days after initial plating. C...

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Bibliographic Details
Published in:Molecular neurodegeneration 1995-03, Vol.4 (1), p.33-41
Main Authors: Couratier, P., Sindou, P., Tabaraud, F., Diop, A.G., Spencer, P.S., Hugon, J.
Format: Article
Language:English
Subjects:
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid - pharmacology
Analysis of Variance
Animals
Calcimycin - pharmacology
Cell Survival - drug effects
Cells, Cultured
Cellular Biology
Dizocilpine Maleate - pharmacology
glutamate
Immunoenzyme Techniques
Life Sciences
metabotropic receptors
Microscopy, Confocal
Neurons - chemistry
NMDA
non-NMDA
Rats
Rats, Wistar
Receptors, AMPA - agonists
Receptors, Metabotropic Glutamate - agonists
Receptors, N-Methyl-D-Aspartate - agonists
Tau protein
tau Proteins - analysis
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Summary:We have analysed changes in tau protein immunoreactivity in rat embryonic neurons degenerating in response to treatment with N-methyl-D-aspartate (NMDA), non-NMDA and metabotropic agonists. Glutamate agonists were applied in a Mg++-free and glycine-supplemented medium 8 days after initial plating. Cell viability was assessed by fluorescein diacetate staining and neuronal survival was evaluated by cell counting. Immunocytochemical and confocal laser microscopic studies used a tau2 monoclonal antibody. Acute and chronic NMDA treatment induced a concentration-dependent increase in intraneuronal tau immunoreactivity. Increased tau immunolabelling during chronic NMDA toxicity was dramatically attenuated by tetrodotoxin and also by 6-cyano-7-nitroquinoxaline-2,3-dione. Non-NMDA and metabotropic receptor agonist treatment produced a weaker augmentation in tau2 immunoreactivity. These findings suggest that, in this model, glutamate-receptor and sodium-channel coactivation are together needed to produce changes in tau immunoreactivity.
ISSN:1055-8330
1750-1326
1522-9661
1750-1326
DOI:10.1006/neur.1995.0004