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Review
. 2009 Apr;88(4):808-15.
doi: 10.1016/j.exer.2009.02.004. Epub 2009 Feb 14.

Neurotrophin roles in retinal ganglion cell survival: lessons from rat glaucoma models

Elaine C Johnson  1 , Ying Guo, William O Cepurna, John C Morrison
Affiliations
Review

Neurotrophin roles in retinal ganglion cell survival: lessons from rat glaucoma models

Elaine C Johnson et al. Exp Eye Res. 2009 Apr.

Abstract

The neurotrophin (NT) hypothesis proposes that the obstruction of retrograde transport at the optic nerve head results in the deprivation of neurotrophic support to retinal ganglion cells (RGC) leading to apoptotic cell death in glaucoma. An important corollary to this concept is the implication that appropriate enhancement of neurotrophic support will prolong the survival of injured RGC indefinitely. This hypothesis is, perhaps, the most widely recognized theory to explain RGC loss resulting from exposure of the eye to elevated intraocular pressure (IOP). Recent studies of NT signaling using rat glaucoma models, have examined the endogenous responses of the retina to pressure exposure as well as studies designed to augment NT signaling in order to rescue RGC from apoptosis following pressure-induced injury. The examination of these studies in this review reveals a number of consistent observations and provides direction for further investigations of this hypothesis.

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Figures

Figure 1
Figure 1
A simplified summary of the NT signaling pathways discussed in this review. NT mediated RGC survival signals are principally mediated via AKT and ERK, while P75NTR is involved in multiple pathways culminating in apoptotic RGC death. However, P75NTR interaction with TRK receptors appears necessary for high affinity ligand binding and P75NTR signaling mediated via NFκB promotes cell survival. Further, P75NTR has plays a key role in RhoA-mediated axon outgrowth inhibition.
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References

    1. Bahr M. Live or let die - retinal ganglion cell death and survival during development and in the lesioned adult CNS. Trends Neurosci. 2000;23(10):483–90. - PubMed
    1. Cellerino A, Carroll P, Thoenen H, Barde YA. Reduced Size of Retinal Ganglion Cell Axons and Hypomyelination in Mice Lacking Brain-Derived Neurotrophic Factor. Mol Cell Neurosci. 1997;5:397–408. - PubMed
    1. Cepurna WO, Johnson EC, Jia L, Morrison JC. Retinal Ganglion Cell Loss in a Glaucoma Model: Does Neurotrophin Deprivation Play a Critical Role? Invest. Ophthalmol Vis Sci. 2007;48(5):3276.
    1. Chen H, Weber AJ. BDNF enhances retinal ganglion cell survival in cats with optic nerve damage. Invest Ophthalmol Vis Sci. 2001;42(5):966–74. - PubMed
    1. Chen H, Weber AJ. Brain-derived neurotrophic factor reduces TrkB protein and mRNA in the normal retina and following optic nerve crush in adult rats. Brain Res. 2004;1011(1):99–106. - PubMed

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