Molecular Neurobiology

, Volume 28, Issue 2, pp 139–147

Retinal remodeling in inherited photoreceptor degenerations


DOI: 10.1385/MN:28:2:139

Cite this article as:
Marc, R.E. & Jones, B.W. Mol Neurobiol (2003) 28: 139. doi:10.1385/MN:28:2:139


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.

Index Entries

Retinitis pigmentosa retinal dystrophies plasticity deafferentiation computational imaging immunocytochemistry amino acids 

Copyright information

© Humana Press Inc 2003

Authors and Affiliations

  1. 1.John A. Moran Eye CenterUniversity of Utah School of MedicineSalt Lake City

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