Inherited Photoreceptor Degeneration Causes the Death of Melanopsin-Positive Retinal Ganglion Cells and Increases Their Coexpression of Brn3a

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Title: Inherited Photoreceptor Degeneration Causes the Death of Melanopsin-Positive Retinal Ganglion Cells and Increases Their Coexpression of Brn3a
Authors: García Ayuso, Diego | Di Pierdomenico, Johnny | Esquiva Sobrino, Gema | Nadal-Nicolás, Francisco Manuel | Pinilla Lozano, Isabel | Cuenca, Nicolás | Vidal Sanz, Manuel | Agudo Barriuso, Marta | Villegas Pérez, María Paz
Research Group/s: Neurobiología del Sistema Visual y Terapia de Enfermedades Neurodegenerativas (NEUROVIS)
Center, Department or Service: Universidad de Alicante. Departamento de Fisiología, Genética y Microbiología
Keywords: P23H | Retinitis pigmentosa | Melanopsin | Brn3a | Automated quantification | Intrinsically photosensitive | Photoreceptor degeneration | Intrinsically photosensitive RGCs
Knowledge Area: Biología Celular
Issue Date: Jul-2015
Publisher: Association for Research in Vision and Ophthalmology (ARVO)
Citation: Investigative Ophthalmology & Visual Science. 2015, 56: 4592-4604. doi:10.1167/iovs.15-16808
Abstract: Purpose: To study the population of intrinsically photosensitive retinal ganglion cells (melanopsin-expressing RGCs, m+RGCs) in P23H-1 rats, a rat model of inherited photoreceptor degeneration. Methods: At postnatal (P) times P30, P365, and P540, retinas from P23H dystrophic rats (line 1, rapid degeneration; and line 3, slow degeneration) and Sprague Dawley (SD) rats (control) were dissected as whole-mounts and immunodetected for melanopsin and/or Brn3a. The dendritic arborization of m+RGCs and the numbers of Brn3a+RGCs and m+RGCs were quantified and their retinal distribution and coexpression analyzed. Results: In SD rats, aging did not affect the population of Brn3a+RGCs or m+RGCs or the percentage that showed coexpression (0.27%). Young P23H-1 rats had a significantly lower number of Brn3a+RGCs and showed a further decline with age. The population of m+RGCs in young P23H-1 rats was similar to that found in SD rats and decreased by 22.6% and 28.2% at P365 and P540, respectively, similarly to the decrease of the Brn3a+RGCs. At these ages the m+RGCs showed a decrease of their dendritic arborization parameters, which was similar in both the P23H-1 and P23H-3 lines. The percentage of coexpression of Brn3a was, however, already significantly higher at P30 (3.31%) and increased significantly with age (10.65% at P540). Conclusions: Inherited photoreceptor degeneration was followed by secondary loss of Brn3a+RGCs and m+RGCs. Surviving m+RGCs showed decreased dendritic arborization parameters and increased coexpression of Brn3a and melanopsin, phenotypic and molecular changes that may represent an effort to resist degeneration and/or preferential survival of m+RGCs capable of synthesizing Brn3a.
Sponsor: Supported by grants from the Spanish Ministry of Economy and Competitiveness: SAF-2012-38328; ISCIII-FEDER “Una manera de hacer Europa” PI13/00643, PI13/01266, and BFU2012-36845, RETICS: RD12/0034/0014, and RD12/0034/0010.
URI: http://hdl.handle.net/10045/57937
ISSN: 0146-0404 (Print) | 1552-5783 (Online)
DOI: 10.1167/iovs.15-16808
Language: eng
Type: info:eu-repo/semantics/article
Rights: © 2015 by Association for Research in Vision and Ophthalmology
Peer Review: si
Publisher version: http://dx.doi.org/10.1167/iovs.15-16808
Appears in Collections:INV - NEUROVIS - Artículos de Revistas

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