Modulation of tau neuronal expression induced by NMDA, non-NMDA and metabotropic glutamate receptor agonists

P. Couratier, P. Sindou, F. Tabaraud, A. G. Diop, P. S. Spencer, Jaques Hugon

Research output: Contribution to journalArticle

18 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)33-41
Number of pages9
JournalNeurodegeneration
Volume4
Issue number1
DOIs
StatePublished - Mar 1995

Keywords

  • Glutamate
  • Metabotropic receptors
  • NMDA
  • Non-NMDA
  • Tau protein

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Neuropsychology and Physiological Psychology
  • Clinical Neurology

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