Apoptosis in the dorsal lateral geniculate nucleus after monocular deprivation involves glutamate signaling, NO production, and PARP activation

Carlo Nucci, Silvia Piccirilli, Paola Rodinò, Robert Nisticò, Marina Grandinetti, Luciano Cerulli, Marcel Leist, Pierluigi Nicotera, Giacinto Bagetta

Research output: Contribution to journalArticlepeer-review

Abstract

In mammals, visual experience during early postnatal life is critical for normal development of the visual system. Here we report that monocular deprivation for 2, 7, and 14 consecutive days causes p53 accumulation, cell death, and progressive loss of neurones in the dorsal lateral geniculate nucleus (dLGN) of newborn rats and these are prevented by NMDA and non-NMDA glutamate receptor antagonists, and by L-NAME, an inhibitor of nitric oxide synthesis. Monocular deprivation also increases dLGN levels of citrulline, the coproduct of nitric oxide synthesis, and this, as well as cell death and neuronal loss, is abolished by antagonists of glutamate receptors and by L-NAME. Finally, poly-(ADP-ribose) polymerase (PARP) knock-out mice appear to be protected from monocular deprivation-induced cell death. In conclusion, during early postnatal development of the rat visual system monocular deprivation causes excitotoxic, nitric oxide-mediated, cell death in the dLGN that appears to be apoptotic and also requires activation of PARP. (C) 2000 Academic Press.

Original languageEnglish
Pages (from-to)360-367
Number of pages8
JournalBiochemical and Biophysical Research Communications
Volume278
Issue number2
DOIs
Publication statusPublished - Nov 19 2000

Keywords

  • N-methyl-D-aspartate receptors (NMDA)
  • Nitric oxide
  • Non-NMDA receptors
  • Poly-(ADP-ribose) polymerase
  • Rat

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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