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Retinal neurodegeneration in experimental glaucoma.
Prog Brain Res. 2015; 220:1-35.PB

Abstract

In rats and mice, limbar tissues of the left eye were laser-photocoagulated (LP) and ocular hypertension (OHT) effects were investigated 1 week to 6 months later. To investigate the innermost layers, retinas were examined in wholemounts using tracing from the superior colliculi to identify retinal ganglion cells (RGCs) with intact retrograde axonal transport, melanopsin immunodetection to identify intrinsically photosensitive RGCs (m(+)RGC), Brn3a immunodetection to identify most RGCs but not m(+)RGCs, RECA1 immunodetection to examine the inner retinal vessels, and DAPI staining to detect all nuclei in the GC layer. The outer retinal layers (ORLs) were examined in cross sections analyzed morphometrically or in wholemounts to study S- and L-cones. Innervation of the superior colliculi was examined 10 days to 14 weeks after LP with orthogradely transported cholera toxin subunit B. By 2 weeks, OHT resulted in pie-shaped sectors devoid of FG(+)RGCs or Brn3a(+)RGCs but with large numbers of DAPI(+)nuclei. Brn3a(+)RGCs were significantly greater than FG(+)RGCs, indicating the survival of large numbers of RGCs with their axonal transport impaired. The inner retinal vasculature showed no abnormalities that could account for the sectorial loss of RGCs. m(+)RGCs decreased to approximately 50-51% in a diffuse loss across the retina. Cross sections showed focal areas of degeneration in the ORLs. RGC loss at 1m diminished to 20-25% and did not progress further with time, whereas the S- and L-cone populations diminished progressively up to 6m. The retinotectal projection was reduced by 10 days and did not progress further. LP-induced OHT results in retrograde degeneration of RGCs and m(+)RGCs, severe damage to the ORL, and loss of retinotectal terminals.

Authors+Show Affiliations

Departamento de Oftalmología, Universidad de Murcia and Instituto Murciano de Investigación Biosanitaria Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain. Electronic address: manuel.vidal@um.es.Departamento de Oftalmología, Universidad de Murcia and Instituto Murciano de Investigación Biosanitaria Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain.Departamento de Oftalmología, Universidad de Murcia and Instituto Murciano de Investigación Biosanitaria Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain.Departamento de Oftalmología, Universidad de Murcia and Instituto Murciano de Investigación Biosanitaria Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain.Departamento de Oftalmología, Universidad de Murcia and Instituto Murciano de Investigación Biosanitaria Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain.Departamento de Oftalmología, Universidad de Murcia and Instituto Murciano de Investigación Biosanitaria Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain.Departamento de Oftalmología, Universidad de Murcia and Instituto Murciano de Investigación Biosanitaria Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain.Departamento de Oftalmología, Universidad de Murcia and Instituto Murciano de Investigación Biosanitaria Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain.Departamento de Oftalmología, Universidad de Murcia and Instituto Murciano de Investigación Biosanitaria Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain.Departamento de Oftalmología, Universidad de Murcia and Instituto Murciano de Investigación Biosanitaria Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain.Departamento de Oftalmología, Universidad de Murcia and Instituto Murciano de Investigación Biosanitaria Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain.

Pub Type(s)

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

Language

eng

PubMed ID

26497783

Citation

Vidal-Sanz, Manuel, et al. "Retinal Neurodegeneration in Experimental Glaucoma." Progress in Brain Research, vol. 220, 2015, pp. 1-35.
Vidal-Sanz M, Valiente-Soriano FJ, Ortín-Martínez A, et al. Retinal neurodegeneration in experimental glaucoma. Prog Brain Res. 2015;220:1-35.
Vidal-Sanz, M., Valiente-Soriano, F. J., Ortín-Martínez, A., Nadal-Nicolás, F. M., Jiménez-López, M., Salinas-Navarro, M., Alarcón-Martínez, L., García-Ayuso, D., Avilés-Trigueros, M., Agudo-Barriuso, M., & Villegas-Pérez, M. P. (2015). Retinal neurodegeneration in experimental glaucoma. Progress in Brain Research, 220, 1-35. https://doi.org/10.1016/bs.pbr.2015.04.008
Vidal-Sanz M, et al. Retinal Neurodegeneration in Experimental Glaucoma. Prog Brain Res. 2015;220:1-35. PubMed PMID: 26497783.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Retinal neurodegeneration in experimental glaucoma. AU - Vidal-Sanz,Manuel, AU - Valiente-Soriano,Francisco J, AU - Ortín-Martínez,Arturo, AU - Nadal-Nicolás,Francisco M, AU - Jiménez-López,Manuel, AU - Salinas-Navarro,Manuel, AU - Alarcón-Martínez,Luis, AU - García-Ayuso,Diego, AU - Avilés-Trigueros,Marcelino, AU - Agudo-Barriuso,Marta, AU - Villegas-Pérez,Maria P, Y1 - 2015/07/02/ PY - 2015/10/27/entrez PY - 2015/10/27/pubmed PY - 2016/11/4/medline KW - Adult rodents KW - Axonal transport KW - BDNF neuroprotection KW - Brn3a KW - Experimental glaucoma KW - Fluorogold KW - Intrinsically photosensitive melanopsin RGCs KW - Laser-induced ocular hypertension KW - Neuronal degeneration KW - S- and L-cones SP - 1 EP - 35 JF - Progress in brain research JO - Prog Brain Res VL - 220 N2 - In rats and mice, limbar tissues of the left eye were laser-photocoagulated (LP) and ocular hypertension (OHT) effects were investigated 1 week to 6 months later. To investigate the innermost layers, retinas were examined in wholemounts using tracing from the superior colliculi to identify retinal ganglion cells (RGCs) with intact retrograde axonal transport, melanopsin immunodetection to identify intrinsically photosensitive RGCs (m(+)RGC), Brn3a immunodetection to identify most RGCs but not m(+)RGCs, RECA1 immunodetection to examine the inner retinal vessels, and DAPI staining to detect all nuclei in the GC layer. The outer retinal layers (ORLs) were examined in cross sections analyzed morphometrically or in wholemounts to study S- and L-cones. Innervation of the superior colliculi was examined 10 days to 14 weeks after LP with orthogradely transported cholera toxin subunit B. By 2 weeks, OHT resulted in pie-shaped sectors devoid of FG(+)RGCs or Brn3a(+)RGCs but with large numbers of DAPI(+)nuclei. Brn3a(+)RGCs were significantly greater than FG(+)RGCs, indicating the survival of large numbers of RGCs with their axonal transport impaired. The inner retinal vasculature showed no abnormalities that could account for the sectorial loss of RGCs. m(+)RGCs decreased to approximately 50-51% in a diffuse loss across the retina. Cross sections showed focal areas of degeneration in the ORLs. RGC loss at 1m diminished to 20-25% and did not progress further with time, whereas the S- and L-cone populations diminished progressively up to 6m. The retinotectal projection was reduced by 10 days and did not progress further. LP-induced OHT results in retrograde degeneration of RGCs and m(+)RGCs, severe damage to the ORL, and loss of retinotectal terminals. SN - 1875-7855 UR - https://www.unboundmedicine.com/medline/citation/26497783/Retinal_neurodegeneration_in_experimental_glaucoma_ DB - PRIME DP - Unbound Medicine ER -