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.
- Metabotropic receptors
- Tau protein
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Neuropsychology and Physiological Psychology
- Clinical Neurology