A tau antisense oligonucleotide decreases neurone sensitivity to excitotoxic injury

Marina Pizzi, Alessandra Valerio, Marina Ribola, Pier Franco Spano, Maurizio Memo

Research output: Contribution to journalArticlepeer-review


Short-term exposure of primary cultures of cerebellar granule cells from neonatal rat brain to high concentrations of glutamate results in neuronal degeneration. We found that glutamate, before causing neuronal degeneration, induced a significant increase of Tau protein immunostaining. Time-course experiments revealed the increase of Tau immunoreactivity to be maximal 2 h after the glutamate pulse. To investigate the possible role of newly synthesized Tau protein in the neurotoxic process activated by glutamate, cerebellar granule cells were preincubated with a specific Tau antisense oligonucleotide. This treatment resulted in (i) an inhibition of the glutamate-induced increase of Tau immunoreactivity and (ii) a decrease in the sensitivity of the neurones to neurotoxic concentrations of glutamate. These data indicate that new synthesis of the cytoskeleton-associated Tau protein is a crucial step in the cascade of events promoted by glutamate and leading to neurodegeneration.

Original languageEnglish
Pages (from-to)823-826
Number of pages4
Issue number6
Publication statusPublished - 1993


  • Antisense oligonucleotide
  • Cerebellar granule cells
  • Glutamate
  • Neurotoxicity
  • Tau

ASJC Scopus subject areas

  • Neuroscience(all)


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