000058389 001__ 58389
000058389 005__ 20210121114532.0
000058389 0247_ $$2doi$$a10.1167/iovs.15-16808
000058389 0248_ $$2sideral$$a92002
000058389 037__ $$aART-2015-92002
000058389 041__ $$aeng
000058389 100__ $$aGarcia-Ayuso D
000058389 245__ $$aInherited photoreceptor degeneration causes the death of melanopsin-positive retinal ganglion cells and increases their coexpression of brn3a
000058389 260__ $$c2015
000058389 5060_ $$aAccess copy available to the general public$$fUnrestricted
000058389 5203_ $$aPurpose: 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.
000058389 536__ $$9info:eu-repo/grantAgreement/ES/ISCIII/PI13-00643$$9info:eu-repo/grantAgreement/ES/ISCIII/PI13-01266$$9info:eu-repo/grantAgreement/ES/ISCIII/RETICS-RD12-0034-0010$$9info:eu-repo/grantAgreement/ES/MICINN/ISCIII-RD12-0034-0014$$9info:eu-repo/grantAgreement/ES/MINECO/BFU2012-36845$$9info:eu-repo/grantAgreement/ES/MINECO/SAF-2012-38328
000058389 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000058389 590__ $$a3.427$$b2015
000058389 591__ $$aOPHTHALMOLOGY$$b6 / 56 = 0.107$$c2015$$dQ1$$eT1
000058389 592__ $$a2.011$$b2015
000058389 593__ $$aOphthalmology$$c2015$$dQ1
000058389 593__ $$aSensory Systems$$c2015$$dQ1
000058389 593__ $$aCellular and Molecular Neuroscience$$c2015$$dQ2
000058389 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000058389 700__ $$aDi Pierdomenico J
000058389 700__ $$aEsquiva G
000058389 700__ $$aNadal-Nicolás FM
000058389 700__ $$0(orcid)0000-0003-0349-9997$$aPinilla I$$uUniversidad de Zaragoza
000058389 700__ $$aCuenca N
000058389 700__ $$aVidal-Sanz M
000058389 700__ $$aAgudo-Barriuso M
000058389 700__ $$aVillegas-Pérez MP.
000058389 7102_ $$11004$$2646$$aUniversidad de Zaragoza$$bDpto. Cirugía,Ginecol.Obstetr.$$cÁrea Oftalmología
000058389 773__ $$g56, 8 (2015), 4592-4604$$pInvestig. ophthalmol. vis. sci.$$tINVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE$$x0146-0404
000058389 8564_ $$s2037843$$uhttps://zaguan.unizar.es/record/58389/files/texto_completo.pdf$$yVersión publicada
000058389 8564_ $$s127462$$uhttps://zaguan.unizar.es/record/58389/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000058389 909CO $$ooai:zaguan.unizar.es:58389$$particulos$$pdriver
000058389 951__ $$a2021-01-21-11:11:06
000058389 980__ $$aARTICLE