A dose-dependent increase of Tau immunostaining is produced by glutamate toxicity in primary neuronal cultures

Brain Res. 1992 Feb 14;572(1-2):242-6. doi: 10.1016/0006-8993(92)90476-p.

Abstract

Neuronal degeneration was produced in primary cultures by glutamate exposure and the modifications of Tau immunoreactivity were analysed in degenerating neurons. After 8-12 days of culture, glutamate was applied at different concentrations (50, 100, 200 and 500 mumol) in a Na(+)- and Mg(2+)-free solution containing calcium. Prior to and 12 hours after glutamate exposure cell death was defined by cell counting in each dish. After fixation, neurons were processed for immunocytochemistry using a Tau2 monoclonal antibody and a Tau polyclonal antibody (Sigma). Tau immunostaining was scored by a blind count of immunoreactive cells and a semi-quantitative evaluation. The results show that the number of labelled neurons and the magnitude of neuronal immunolabelling are both related to the glutamate concentration. Our findings indicate that glutamate induces a dose-dependent increase of Tau immunoreactivity directly related to its cellular action on neuronal cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / physiopathology*
  • Animals
  • Cells, Cultured
  • Cerebral Cortex / chemistry
  • Cerebral Cortex / cytology
  • Cerebral Cortex / drug effects*
  • Glutamates / toxicity*
  • Glutamic Acid
  • Immunohistochemistry
  • Nerve Degeneration / drug effects*
  • Neurons / chemistry
  • Neurons / drug effects*
  • Rats
  • tau Proteins / analysis*

Substances

  • Glutamates
  • tau Proteins
  • Glutamic Acid