April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Morphological Characterization of the Retinal Degeneration in Two Rat Models for Retinitis Pigmentosa: P23H-1 and S334ter-3 Rhodopsin Mutations
Author Affiliations & Notes
  • J. Kaur
    Division of Ophthalmology, Centre for Ophthalmology, Tuebingen, Germany
  • S. Bolz
    Division of Ophthalmology, Centre for Ophthalmology, Tuebingen, Germany
  • T. van Veen
    Division of Ophthalmology, Centre for Ophthalmology, Tuebingen, Germany
  • B. Arango-Gonzalez
    Division of Ophthalmology, Centre for Ophthalmology, Tuebingen, Germany
  • Footnotes
    Commercial Relationships  J. Kaur, None; S. Bolz, None; T. van Veen, None; B. Arango-Gonzalez, None.
  • Footnotes
    Support  Foundation Fighting Blindness (FFB); Tistou und Charlotte Kerstan Stiftung; Transgenic animals were kindly provided by Dr. M.M. La Vail (UCSF, San Fransisco, CA)
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 2291. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      J. Kaur, S. Bolz, T. van Veen, B. Arango-Gonzalez; Morphological Characterization of the Retinal Degeneration in Two Rat Models for Retinitis Pigmentosa: P23H-1 and S334ter-3 Rhodopsin Mutations. Invest. Ophthalmol. Vis. Sci. 2009;50(13):2291.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Purpose: : The goal of this study was to investigate structural changes and expression of different cell markers in the retinas of two different rat models, P23H and S334ter, homologous for human autosomal dominant retinitis pigmentosa.

Methods: : Retinas from heterozygous P23H-1 and S334ter-3, and CD rats were collected at various postnatal ages (PN0 - PN30). Tissues were examined by conventional histological techniques and immunostained with cell-type-specific markers.

Results: : Histological examination revealed the rapid and continuous retinal degeneration of S334ter-3 and the comparatively slower degeneration in P23H-1 rats. The S334ter-3 retina does not reach a normal postnatal development, as evident by rhodopsin staining, that no outer segments (OS) of photoreceptors are present at any stage of development. At PN30, rhodopsin staining showed no remaining rods, therefore, we can confirm that only cones are present in the ONL at this age. In the P23H-1 mutants, however, fully developed OS were present before degeneration began. In both models, expression of calretinin in amacrine and ganglion cells was not modified compared with CD retinae. In both mutants staining of rod-bipolar and amacrine cells by PKC was similar to CD rats but the staining intensity of their axons within the IPL was decreased at PN30. PKC labelling of S-cones in S334ter-3 animals was detected only between PN10 and 12 and then disappeared. In P23H-1 rats this staining was still present at PN30 but the OS appeared shorter than in CD retinas. Even though the number of photoreceptors was reduced, the pattern of bipolar cells expressing recoverin was unchanged in both mutants. An increased Glutamine synthetase expression, restricted to Müller cells, was apparent in both the S334ter-3 and P23H-1 retinas. Moreover, an upregulation of glial fibrillary acidic protein was observed in both transgenic rat models.

Conclusions: : At least until PN30, the development of the inner retina is not profoundly altered in both transgenic models. S334ter-3 and P23H-1 rats are valuable tools to test potential treatments for early and late forms of RP.

Keywords: photoreceptors • retinal degenerations: cell biology • immunohistochemistry 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×