4.5 Article

Functional and structural modifications during retinal degeneration in the rd10 mouse

Journal

NEUROSCIENCE
Volume 155, Issue 3, Pages 698-713

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2008.06.042

Keywords

retina; rod; cone; bipolar cells; phosphodiesterase; apoptosis

Categories

Funding

  1. Spanish Ministerio de Educacion y Ciencia [SAF200405870, SAF2007-66175, BF12003-01404, BFU2006-00957]
  2. Ministerio de Sanidad [RETICS RD0710062]
  3. Comunidad de Madrid [08.5-0019.112001, 08.5-00491 2003]
  4. Ministerio de Educacion y Ciencia

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Mouse models of retinal degeneration are useful tools to study therapeutic approaches for patients affected by hereditary retinal dystrophies. We have studied degeneration in the rd10 mice both by immunocytochemistry and TUNEL-labeling of retinal cells, and through electrophysiological recordings. The cell degeneration in the retina of rd10 mice produced appreciable morphological changes in rod and cone cells by P20. Retinal cell death is clearly observed in the central retina and it peaked at P25 when there were 800 TUNEL-positive cells per MM2. In the central retina, only one row of photoreceptors remained in the outer nuclear layer by P40 and there was a remarkable deterioration of bipolar cell dendrites postsynaptic to photoreceptors. The axon terminals of bipolar cells also underwent atrophy and the inner retina was subject to further changes, including a reduction and disorganization of All amacrine cell population. Glutamate sensitivity was tested in rod bipolar cells with the single cell patch-clamp technique in slice preparations, although at P60 no significant differences were observed with agematched controls. Thus, we conclude that rod and cone degeneration in the rd10 mouse model is followed by deterioration of their postsynaptic cells and the cells in the inner retina. However, the functional preservation of receptors for photoreceptor transmission in bipolar cells may open new therapeutic possibilities. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.

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