Open AccessThe visual response of retinal ganglion cells is not altered by optic nerve transection in transgenic mice overexpressing Bcl-2
Author(s) -
Vittorio Porciatti,
Tommaso Pizzorusso,
Maria Cristina Cenni,
Lamberto Maffei
Publication year - 1996
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.93.25.14955
Subject(s) - axotomy , biology , retinal ganglion cell , ganglion , optic nerve , retina , microbiology and biotechnology , neuroscience , regeneration (biology) , programmed cell death , genetically modified mouse , retinal , apoptosis , giant retinal ganglion cells , transgene , retinal degeneration , biochemistry , gene
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 deathin 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.