<?xml version="1.0" encoding="UTF-8"?>
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<dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:invenio="http://invenio-software.org/elements/1.0" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><dc:identifier>doi:10.1167/iovs.15-16808</dc:identifier><dc:language>eng</dc:language><dc:creator>Garcia-Ayuso D</dc:creator><dc:creator>Di Pierdomenico J</dc:creator><dc:creator>Esquiva G</dc:creator><dc:creator>Nadal-Nicolás FM</dc:creator><dc:creator>Pinilla I</dc:creator><dc:creator>Cuenca N</dc:creator><dc:creator>Vidal-Sanz M</dc:creator><dc:creator>Agudo-Barriuso M</dc:creator><dc:creator>Villegas-Pérez MP.</dc:creator><dc:title>Inherited photoreceptor degeneration causes the death of melanopsin-positive retinal ganglion cells and increases their coexpression of brn3a</dc:title><dc:identifier>ART-2015-92002</dc:identifier><dc:description>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.</dc:description><dc:date>2015</dc:date><dc:source>http://zaguan.unizar.es/record/58389</dc:source><dc:doi>10.1167/iovs.15-16808</dc:doi><dc:identifier>http://zaguan.unizar.es/record/58389</dc:identifier><dc:identifier>oai:zaguan.unizar.es:58389</dc:identifier><dc:relation>info:eu-repo/grantAgreement/ES/ISCIII/PI13-00643</dc:relation><dc:relation>info:eu-repo/grantAgreement/ES/ISCIII/PI13-01266</dc:relation><dc:relation>info:eu-repo/grantAgreement/ES/ISCIII/RETICS-RD12-0034-0010</dc:relation><dc:relation>info:eu-repo/grantAgreement/ES/MICINN/ISCIII-RD12-0034-0014</dc:relation><dc:relation>info:eu-repo/grantAgreement/ES/MINECO/BFU2012-36845</dc:relation><dc:relation>info:eu-repo/grantAgreement/ES/MINECO/SAF-2012-38328</dc:relation><dc:identifier.citation>INVESTIGATIVE OPHTHALMOLOGY &amp; VISUAL SCIENCE 56, 8 (2015), 4592-4604</dc:identifier.citation><dc:rights>by</dc:rights><dc:rights>http://creativecommons.org/licenses/by/3.0/es/</dc:rights><dc:rights>info:eu-repo/semantics/openAccess</dc:rights></dc:dc>

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