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Inherited Photoreceptor Degeneration Causes the Death of Melanopsin-Positive Retinal Ganglion Cells and Increases Their Coexpression of Brn3a.
Invest Ophthalmol Vis Sci. 2015 Jul; 56(8):4592-604.IO

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.

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Publisher Full Text (DOI)

Authors+Show Affiliations

García-Ayuso D
Instituto Murciano de Investigación Biosanitaria Hospital Virgen de la Arrixaca (IMIB-Virgen de la Arrixaca) and Departamento de Oftalmología, Facultad de Medicina, Universidad de Murcia, Murcia, Spain.
Di Pierdomenico J
Instituto Murciano de Investigación Biosanitaria Hospital Virgen de la Arrixaca (IMIB-Virgen de la Arrixaca) and Departamento de Oftalmología, Facultad de Medicina, Universidad de Murcia, Murcia, Spain.
Esquiva G
Departamento de Fisiología, Genética y Microbiología, Universidad de Alicante, San Vicente del Raspeig, Alicante, Spain.
Nadal-Nicolás FM
Instituto Murciano de Investigación Biosanitaria Hospital Virgen de la Arrixaca (IMIB-Virgen de la Arrixaca) and Departamento de Oftalmología, Facultad de Medicina, Universidad de Murcia, Murcia, Spain.
Pinilla I
Servicio de Oftalmología, Hospital Clínico Universitario Lozano Blesa, Zaragoza, Spain.
Cuenca N
Departamento de Fisiología, Genética y Microbiología, Universidad de Alicante, San Vicente del Raspeig, Alicante, Spain.
Vidal-Sanz M
Instituto Murciano de Investigación Biosanitaria Hospital Virgen de la Arrixaca (IMIB-Virgen de la Arrixaca) and Departamento de Oftalmología, Facultad de Medicina, Universidad de Murcia, Murcia, Spain.
Agudo-Barriuso M
Instituto Murciano de Investigación Biosanitaria Hospital Virgen de la Arrixaca (IMIB-Virgen de la Arrixaca) and Departamento de Oftalmología, Facultad de Medicina, Universidad de Murcia, Murcia, Spain.
Villegas-Pérez MP
Instituto Murciano de Investigación Biosanitaria Hospital Virgen de la Arrixaca (IMIB-Virgen de la Arrixaca) and Departamento de Oftalmología, Facultad de Medicina, Universidad de Murcia, Murcia, Spain.

MeSH

AnimalsCell DeathDisease Models, AnimalGene Expression RegulationImmunoenzyme TechniquesPhotoreceptor Cells, VertebrateRatsRats, Sprague-DawleyRats, TransgenicRetinal DegenerationRetinal Ganglion CellsRod OpsinsTranscription Factor Brn-3A

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26200499

Citation

García-Ayuso, Diego, et al. "Inherited Photoreceptor Degeneration Causes the Death of Melanopsin-Positive Retinal Ganglion Cells and Increases Their Coexpression of Brn3a." Investigative Ophthalmology & Visual Science, vol. 56, no. 8, 2015, pp. 4592-604.
García-Ayuso D, Di Pierdomenico J, Esquiva G, et al. Inherited Photoreceptor Degeneration Causes the Death of Melanopsin-Positive Retinal Ganglion Cells and Increases Their Coexpression of Brn3a. Invest Ophthalmol Vis Sci. 2015;56(8):4592-604.
García-Ayuso, D., Di Pierdomenico, J., Esquiva, G., Nadal-Nicolás, F. M., Pinilla, I., Cuenca, N., Vidal-Sanz, M., Agudo-Barriuso, M., & Villegas-Pérez, M. P. (2015). Inherited Photoreceptor Degeneration Causes the Death of Melanopsin-Positive Retinal Ganglion Cells and Increases Their Coexpression of Brn3a. Investigative Ophthalmology & Visual Science, 56(8), 4592-604. https://doi.org/10.1167/iovs.15-16808
García-Ayuso D, et al. Inherited Photoreceptor Degeneration Causes the Death of Melanopsin-Positive Retinal Ganglion Cells and Increases Their Coexpression of Brn3a. Invest Ophthalmol Vis Sci. 2015;56(8):4592-604. PubMed PMID: 26200499.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inherited Photoreceptor Degeneration Causes the Death of Melanopsin-Positive Retinal Ganglion Cells and Increases Their Coexpression of Brn3a. AU - García-Ayuso,Diego, AU - Di Pierdomenico,Johnny, AU - Esquiva,Gema, AU - Nadal-Nicolás,Francisco Manuel, AU - Pinilla,Isabel, AU - Cuenca,Nicolás, AU - Vidal-Sanz,Manuel, AU - Agudo-Barriuso,Marta, AU - Villegas-Pérez,María P, PY - 2015/7/23/entrez PY - 2015/7/23/pubmed PY - 2015/10/16/medline SP - 4592 EP - 604 JF - Investigative ophthalmology & visual science JO - Invest Ophthalmol Vis Sci VL - 56 IS - 8 N2 - 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. SN - 1552-5783 UR - https://www.unboundmedicine.com/medline/citation/26200499/Inherited_Photoreceptor_Degeneration_Causes_the_Death_of_Melanopsin_Positive_Retinal_Ganglion_Cells_and_Increases_Their_Coexpression_of_Brn3a_ DB - PRIME DP - Unbound Medicine ER -