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.

Nucci, C., Piccirilli, S., Rodinò, P., Nistico', R.g., Grandinetti, M., Cerulli, L., et al. (2000). Apoptosis in the dorsal lateral geniculate nucleus after monocular deprivation involves glutamate signaling, NO production, and PARP activation. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 278(2), 360-367 [10.1006/bbrc.2000.3811].

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

NUCCI, CARLO;PICCIRILLI, SILVIA;NISTICO', ROBERT GIOVANNI;CERULLI, LUCIANO;
2000-11-19

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.
19-nov-2000
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore BIO/14 - FARMACOLOGIA
Settore MED/30 - MALATTIE APPARATO VISIVO
English
Animals; Apoptosis; Rats, Long-Evans; Enzyme Activation; Glutamic Acid; Receptors, Glutamate; Geniculate Bodies; Nitric Oxide; Rats; Animals, Newborn; Nitric Oxide Synthase; Poly(ADP-ribose) Polymerases; Immunohistochemistry; Signal Transduction
Nucci, C., Piccirilli, S., Rodinò, P., Nistico', R.g., Grandinetti, M., Cerulli, L., et al. (2000). Apoptosis in the dorsal lateral geniculate nucleus after monocular deprivation involves glutamate signaling, NO production, and PARP activation. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 278(2), 360-367 [10.1006/bbrc.2000.3811].
Nucci, C; Piccirilli, S; Rodinò, P; Nistico', Rg; Grandinetti, M; Cerulli, L; Leist, M; Nicotera, P; Bagetta, G
Articolo su rivista
File in questo prodotto:
File Dimensione Formato  
BBRC'00apopLGN.pdf

solo utenti autorizzati

Descrizione: Apoptosis in the dorsal lateral geniculate nucleus after monocular deprivation involves glutamate signaling, NO production, and PARP activation
Licenza: Copyright dell'editore
Dimensione 247 kB
Formato Adobe PDF
247 kB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/64714
Citazioni
  • ???jsp.display-item.citation.pmc??? 2
  • Scopus 19
  • ???jsp.display-item.citation.isi??? 18
social impact