Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2003 Oct;28(2):139-47.
doi: 10.1385/MN:28:2:139.

Retinal Remodeling in Inherited Photoreceptor Degenerations

Affiliations

Retinal Remodeling in Inherited Photoreceptor Degenerations

Robert E Marc et al. Mol Neurobiol. .

Abstract

Photoreceptor degenerations initiated in rods or the retinal pigmented epithelium usually evoke secondary cone death and sensory deafferentation of the surviving neural retina. In the mature central nervous system, deafferentation evokes atrophy and connective re-patterning. It has been assumed that the neural retina does not remodel, and that it is a passive survivor. Screening of advanced stages of human and rodent retinal degenerations with computational molecular phenotyping has exposed a prolonged period of aggressive negative remodeling in which neurons migrate along aberrant glial columns and seals, restructuring the adult neural retina (1). Many neurons die, but survivors rewire the remnant inner plexiform layer (IPL), forming thousands of novel ectopic microneuromas in the remnant inner nuclear layer (INL). Bipolar and amacrine cells engage in new circuits that are most likely corruptive. Remodeling in human and rodent retinas emerges regardless of the molecular defects that initially trigger retinal degenerations. Although remodeling may constrain therapeutic intervals for molecular, cellular, or bionic rescue, the exposure of intrinsic retinal remodeling by the removal of sensory control in retinal degenerations suggests that neuronal organization in the normal retina may be more plastic than previously believed.

Similar articles

See all similar articles

Cited by 75 articles

See all "Cited by" articles

References

    1. JAMA. 2000 May 3;283(17):2297 - PubMed
    1. Invest Ophthalmol Vis Sci. 1978 Aug;17(8):762-8 - PubMed
    1. Eye (Lond). 2002 Jul;16(4):375-87 - PubMed
    1. Neurosci Lett. 1997 Mar 28;225(1):13-6 - PubMed
    1. Science. 2002 Feb 8;295(5557):1022-5 - PubMed

Publication types

MeSH terms

LinkOut - more resources

Feedback