The visual response of retinal ganglion cells is not altered by optic nerve transection in transgenic mice overexpressing Bcl-2

Vittorio Porciatti, T. Pizzorusso, M. C. Cenni, L. Maffei

Research output: Contribution to journalArticle

77 Citations (Scopus)

Abstract

Attempts to rescue retinal ganglion cells from retrograde degeneration have had limited success, and the residual function of surviving neurons is not known. Recently, it has been found that axotomized retinal ganglion cells die by apoptotic mechanisms. We have used adult transgenic mice overexpressing the Bcl-2 protein, a powerful inhibitor of apoptosis, as a model for preventing injury-induced cell death in vivo. Several months after axotomy, the majority of retinal ganglion cells survived and exhibited normal visual responses. In control wild-type mice, the vast majority of axotomized retinal ganglion cells degenerated, and the physiological responses were abolished, These results suggest that strategies aimed at increasing Bcl-2 expression, or mimicking its function, might effectively counteract trauma- induced cell death in the central nervous system. Neuronal survival is a necessary condition in the challenge for promoting regeneration and eventually restoring neuronal function.

Original languageEnglish
Pages (from-to)14955-14959
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume93
Issue number25
DOIs
StatePublished - Dec 10 1996
Externally publishedYes

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Optic Nerve Injuries
Retinal Ganglion Cells
Transgenic Mice
Cell Death
Retrograde Degeneration
Axotomy
Wounds and Injuries
Regeneration
Central Nervous System
Apoptosis
Neurons
Proteins

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

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abstract = "Attempts to rescue retinal ganglion cells from retrograde degeneration have had limited success, and the residual function of surviving neurons is not known. Recently, it has been found that axotomized retinal ganglion cells die by apoptotic mechanisms. We have used adult transgenic mice overexpressing the Bcl-2 protein, a powerful inhibitor of apoptosis, as a model for preventing injury-induced cell death in vivo. Several months after axotomy, the majority of retinal ganglion cells survived and exhibited normal visual responses. In control wild-type mice, the vast majority of axotomized retinal ganglion cells degenerated, and the physiological responses were abolished, These results suggest that strategies aimed at increasing Bcl-2 expression, or mimicking its function, might effectively counteract trauma- induced cell death in the central nervous system. Neuronal survival is a necessary condition in the challenge for promoting regeneration and eventually restoring neuronal function.",
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