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13. Chronobiotic effect of melatonin in experimental optic neuritis

Author

Aranda, Marcos L., primary, Narvaez, Omar, additional, Altschuler, Florencia, additional, Calanni, Juan S., additional, González Fleitas, María F., additional, Sande, Pablo H., additional, Dorfman, Damián, additional, Concha, Luis, additional, and Rosenstein, Ruth E., additional

Published
2021
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16. Melatonin protects the retina from experimental nonexudative age‐related macular degeneration in mice

Author

Diéguez, Hernán H., primary, González Fleitas, María F., additional, Aranda, Marcos L., additional, Calanni, Juan S., additional, Keller Sarmiento, María I., additional, Chianelli, Mónica S., additional, Alaimo, Agustina, additional, Sande, Pablo H., additional, Romeo, Horacio E., additional, Rosenstein, Ruth E., additional, and Dorfman, Damián, additional

Published
2020
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18. Therapeutic benefit of environmental enrichment on optic neuritis

Author

Aranda, Marcos L., primary, González Fleitas, María F., additional, Dieguez, Hernán H., additional, Milne, Georgia A., additional, Devouassoux, Julián D., additional, Keller Sarmiento, María I., additional, Chianelli, Mónica, additional, Sande, Pablo H., additional, Dorfman, Damián, additional, and Rosenstein, Ruth E., additional

Published
2019
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20. Enriched environment provides neuroprotection against experimental glaucoma.

Author

González Fleitas, María F., Devouassoux, Julián D., Aranda, Marcos L., Calanni, Juan S., Chianelli, Monica S., Dorfman, Damián, and Rosenstein, Ruth E.

Subjects
ANTERIOR chamber (Eye), OLIGODENDROGLIA, RETINAL ganglion cells, VISUAL evoked potentials, GLAUCOMA, BRAIN-derived neurotrophic factor, OPTIC nerve
Abstract

Glaucoma is one of the most frequent causes of visual impairment worldwide, and involves selective damage to retinal ganglion cells (RGCs) and their axons. We analyzed the effect of enriched environment (EE) housing on the optic nerve, and retinal alterations in an induced model of ocular hypertension. For this purpose, male Wistar rats were weekly injected with vehicle or chondroitin sulfate (CS) into the eye anterior chamber for 10 weeks and housed in standard environment or EE. EE housing prevented the effect of experimental glaucoma on visual evoked potentials, retinal anterograde transport, phosphorylated neurofilament‐immunoreactivity, axon number, microglial/macrophage reactivity (ionized calcium binding adaptor molecule 1‐immunoreactivity), and astrocytosis (glial fibrillary acidic protein‐immunostaining), as well as oligodendrocytes alterations (luxol fast blue staining, and myelin basic protein‐immunoreactivity) in the proximal portion of the optic nerve. Moreover EE prevented the increase in ionized calcium binding adaptor molecule‐1 levels, and RGC loss (Brn3a‐immunoreactivity) in the retina from hypertensive eyes. EE increased retinal brain‐derived neurotrophic factor levels. When EE housing started after 6 weeks of ocular hypertension, a preservation of visual evoked potentials amplitude, axon, and Brn3a(+) RGC number was observed. Taken together, these results suggest that EE preserved visual functions, reduced optic nerve axoglial alterations, and protected RGCs against glaucomatous damage. [ABSTRACT FROM AUTHOR]

Published
2020
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21. Neuroprotective effect of melatonin in experimental optic neuritis in rats

Author

Aranda, Marcos Luis, González Fleitas, María Florencia, de Laurentiis, Andrea, Keller Sarmiento, María Inés, Chianelli, Mónica Silvia, Sande Casal, Pablo Horacio, Dorfman, Damián, and Rosenstein, Ruth Estela

Subjects
Retinal Ganglion Cells, Medicina Básica, Optic Neuritis, CIENCIAS MÉDICAS Y DE LA SALUD, Pupil Light Reflex, Visual Evoked Potentials, Patología, Axoglial Alterations, Melatonin
Abstract

Optic neuritis (ON) is an inflammatory, demyelinating, and neurodegenerative condition of the optic nerve, which might induce permanent vision loss. Currently, there are no effective therapies for this disorder. We have developed an experimental model of primary ON in rats through a single microinjection of 4.5 μg of bacterial lipopolysaccharide (LPS) into the optic nerve. Since melatonin acts as a pleiotropic therapeutic agent in various neurodegenerative diseases, we analyzed the effect of melatonin on LPS-induced ON. For this purpose, LPS or vehicle were injected into the optic nerve from adult male Wistar rats. One group of animals received a subcutaneous pellet of 20 mg melatonin at 24 hr before vehicle or LPS injection, and another group was submitted to a sham procedure. Melatonin completely prevented the decrease in visual evoked potentials (VEPs), and pupil light reflex (PLR), and preserved anterograde transport of cholera toxin β-subunit from the retina to the superior colliculus. Moreover, melatonin prevented microglial reactivity (ED1-immunoreactivity, P < 0.01), astrocytosis (glial fibrillary acid protein-immunostaining, P < 0.05), demyelination (luxol fast blue staining, P < 0.01), and axon (toluidine blue staining, P < 0.01) and retinal ganglion cell (Brn3a-immunoreactivity, P < 0.01) loss, induced by LPS. Melatonin completely prevented the increase in nitric oxide synthase 2, cyclooxygenase-2 levels (Western blot) and TNFα levels, and partly prevented lipid peroxidation induced by experimental ON. When the pellet of melatonin was implanted at 4 days postinjection of LPS, it completely reversed the decrease in VEPs and PLR. These data suggest that melatonin could be a promising candidate for ON treatment. Fil: Aranda, Marcos Luis. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: González Fleitas, María Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: de Laurentiis, Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Keller Sarmiento, María Inés. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Chianelli, Mónica Silvia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Sande Casal, Pablo Horacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Dorfman, Damián. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Rosenstein, Ruth Estela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina

Published
2016

25. Treatment with melatonin after onset of experimental uveitis attenuates ocular inflammation

Author

Sande, Pablo Horacio, Dorfman, Damián, Fernandez, Diego Carlos, Chianelli, Monica Silvia, Domínguez Rubio, Ana Paula, Franchi, Ana Maria, Silberman, Dafne Magali, Rosenstein, Ruth Estela, and Saenz, Daniel Alberto

Subjects
Otras Ciencias de la Salud, purl.org/becyt/ford/3.3 [https], CIENCIAS MÉDICAS Y DE LA SALUD, ocular inflammation, Ciencias de la Salud, melatonin, purl.org/becyt/ford/3 [https]
Abstract

Background and Purpose: Uveitis is a prevalent intraocular inflammatory disease and one of the most damaging ocular conditions. Pretreatment with melatonin prevented ocular inflammation induced by an intravitreal injection of bacterial LPS in the Syrian hamster. Here, we have assessed the anti-inflammatory effects of melatonin administered after the onset of ocular inflammation. Experimental Approach: The eyes of male Syrian hamsters were intravitreally injected with vehicle or LPS. Melatonin was injected i.p. every 24 h, starting 12 or 24 h after the LPS injection. A clinical evaluation (with a score index based on clinical symptoms), the number of infiltrating cells, protein concentration and PGE2 and PGF2α levels in the aqueous humour, as well as retinal NOS activity, lipid peroxidation and TNF-α levels were assessed. Retinal function was assessed by scotopic electroretinography, and light microscopy and immunohistochemistry were used to evaluate the state of the retinal structure. Key Results: Both treatment regimens with melatonin decreased clinical symptoms, reduced the leakage of cells and proteins, and decreased PG levels in aqueous humour from eyes injected with LPS. In addition, melatonin treatment blocked the decrease in scotopic electroretinogram a- and b-wave amplitude, protected the retinal structure and reduced the increase in NOS activity, lipid peroxidation and TNF-α levels, induced by LPS. Conclusions and Implications: These results indicate that treatment with melatonin, starting after the onset of uveitis, attenuated ocular inflammation induced by LPS in the Syrian hamster and support the use of melatonin as a therapeutic resource for uveitis treatment. Fil: Sande, Pablo Horacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Dorfman, Damián. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Fernandez, Diego Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Chianelli, Monica Silvia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Domínguez Rubio, Ana Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Franchi, Ana Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Silberman, Dafne Magali. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Rosenstein, Ruth Estela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Saenz, Daniel Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina

Published
2014

26. Global and Ocular Hypothermic Preconditioning Protect the Rat Retina from Ischemic Damage

Author

Salido, Ezequiel Martin, Dorfman, Damián, Bordone, Melina Paula, Chianelli, Monica Silvia, González Fleitas, María Florencia, and Rosenstein, Ruth Estela

Subjects
Ciencias Médicas y de la Salud, Medicina Básica, Neurociencias (incluye Psicofiosiología), preconditioning, purl.org/becyt/ford/3 [https], purl.org/becyt/ford/3.1 [https], sense organs, hypothermia, eye diseases, ischemia retinal
Abstract

Retinal ischemia could provoke blindness. At present, there is no effective treatment against retinal ischemic damage. Strong evidence supports that glutamate is implicated in retinal ischemic damage. We investigated whether a brief period of global or ocular hypothermia applied 24 h before ischemia (i.e. hypothermic preconditioning, HPC) protects the retina from ischemia/reperfusion damage, and the involvement of glutamate in the retinal protection induced by HPC. For this purpose, ischemia was induced by increasing intraocular pressure to 120 mm Hg for 40 min. One day before ischemia, animals were submitted to global or ocular hypothermia (33uC and 32uC for 20 min, respectively) and fourteen days after ischemia, animals were subjected to electroretinography and histological analysis. Global or ocular HPC afforded significant functional (electroretinographic) protection in eyes exposed to ischemia/reperfusion injury. A marked alteration of the retinal structure and a decrease in retinal ganglion cell number were observed in ischemic retinas, whereas global or ocular HPC significantly preserved retinal structure and ganglion cell count. Three days after ischemia, a significant decrease in retinal glutamate uptake and glutamine synthetase activity was observed, whereas ocular HPC prevented the effect of ischemia on these parameters. The intravitreal injection of supraphysiological levels of glutamate induced alterations in retinal function and histology which were significantly prevented by ocular HPC. These results support that global or ocular HPC significantly protected retinal function and histology from ischemia/reperfusion injury, probably through a glutamatedependent mechanism. Fil: Salido E. Fil: Dorfman D. Fil: Bordone, Melina. Fil: Chianelli Mónica S. Fil: González Fleitas Mf. Fil: Rosenstein Re.

Published
2013

28. Efecto terapéutico de la melatonina en la uveítis experimental

Author

Sande, Pablo Horacio, Fernández, Diego Carlos, Chianelli, Mónica Silvia, Silberman, Dafne Magalí, de Zavalía, Nuria María Asunción, Belforte, Nicolás Adalberto, Salido, Ezequiel Martín, Franco, Pablo Javier, Dorfman, Damián, Lanzani, María Florencia, Bordone, Melina Paula, Keller Sarmiento, María Inés, Saenz, Daniel Alberto, and Rosenstein, Ruth Estela

Subjects
Melatonina, Uveitis, Barrera hemato-ocular, Medicina Básica, CIENCIAS MÉDICAS Y DE LA SALUD, Neurociencias, Lipopolisacárido bacteriano, Modelo experimental
Abstract

Objetivos: Analizar el efecto de la melatonina en la uveítis inducida por una inyección intravítrea de lipopolisacárido bacteriano (LPS) en el hámster dorado. Métodos: Se implantó un pellet de melatonin dos horas antes de la inyección de LPS. La respuesta inflamatoria se evaluó en términos de: i) integridad de la barrera hemato-ocular, ii) signos clínicos, iii) estudios histopatológicos, y iv) función retiniana. Resultados: La melatonina disminuyó los signos clínicos y la infiltración de proteínas y células en el segmento anterior, protegió la ultraestructura de las barreras hemato-oculares y los fotorreceptores, previno la disfunción electrorretinográfica, y el aumento de la actividad retiniana de NOS y de TNF inducidos por LPS. La melatonina disminuyó el efecto del LPS sobre los niveles nucleares de las subunidades p50 y p65 del factor nuclear B. Conclusiones: La melatonina podría constituir una nueva estrategia terapéutica para el tratamiento de la uveítis. Objective: To analyze the therapeutic effect of melatonin on uveitis induced by an intravitreal injection of bacterial lipopolysaccharide (LPS) in the golden hamster. Methods: A pellet of melatonin was implanted subcutaneously two hours before the injection of LPS. One and eight days after injections, the inflammatory response was evaluated in terms of: i) integrity of blood-ocular barrier, ii) clinical signs, iii) histopathological studies, and iv) retinal function. Results: Melatonin reduced the leakage of proteins and cells in the anterior segment of LPS-injected eyes, decreased clinical signs and protected the ultrastructure of blood-ocular barriers, and photoreceptors. Melatonin prevented the decrease in the electroretinographic activity induced by LPS. Melatonin significantly abrogated the LPS-induced increase in retinal NOS activity, tumor necrosis factor (TNF), and nuclear factor B (NFB) p50 and p65 subunits levels. Conclusions: These results support the use of melatonin as a new therapeutic strategy for the treatment of uveitis. Fil: Sande, Pablo Horacio. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina Fil: Fernández, Diego Carlos. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Chianelli, Mónica Silvia. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Silberman, Dafne Magalí. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: de Zavalía, Nuria María Asunción. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Belforte, Nicolás Adalberto. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Salido, Ezequiel Martín. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Franco, Pablo Javier. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina Fil: Dorfman, Damián. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Lanzani, María Florencia. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina Fil: Bordone, Melina Paula. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Keller Sarmiento, María Inés. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Saenz, Daniel Alberto. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina Fil: Rosenstein, Ruth Estela. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina

Published
2009

37. Effect of retinal ischemia on the non-image forming visual system.

Author

González Fleitas, María Florencia, Bordone, Melina, Rosenstein, Ruth E., and Dorfman, Damián

Subjects
RETINAL injuries, ISCHEMIA, VISION disorders, RETINAL ganglion cells, PHOTOSYNTHETIC pigments, MELANOPSIN, OPTICAL reflection
Abstract

Retinal ischemic injury is an important cause of visual impairment. The loss of retinal ganglion cells (RGCs) is a key sign of retinal ischemic damage. A subset of RGCs expressing the photopigment melanopsin (mRGCs) regulates non-image-forming visual functions such as the pupillary light reflex (PLR), and circadian rhythms. We studied the effect of retinal ischemia on mRGCs and the non-image-forming visual system function. For this purpose, transient ischemia was induced by raising intraocular pressure to 120 mm Hg for 40 min followed by retinal reperfusion by restoring normal pressure. At 4 weeks post-treatment, animals were subjected to electroretinography and histological analysis. Ischemia induced a significant retinal dysfunction and histological alterations. At this time point, a significant decrease in the number of Brn3a(+) RGCs and in the anterograde transport from the retina to the superior colliculus and lateral geniculate nucleus was observed, whereas no differences in the number of mRGCs, melanopsin levels, and retinal projections to the suprachiasmatic nuclei and the olivary pretectal nucleus were detected. At low light intensity, a decrease in pupil constriction was observed in intact eyes contralateral to ischemic eyes, whereas at high light intensity, retinal ischemia did not affect the consensual PLR. Animals with ischemia in both eyes showed a conserved locomotor activity rhythm and a photoentrainment rate which did not differ from control animals. These results suggest that the non-image forming visual system was protected against retinal ischemic damage. [ABSTRACT FROM AUTHOR]

Published
2015
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38. Superior cervical gangliectomy induces non-exudative age-related macular degeneration in mice

Author

Dieguez, Hernán H., Romeo, Horacio E., González Fleitas, María F., Aranda, Marcos L., Milne, Georgia A., Rosenstein, Ruth E., and Dorfman, Damián

Abstract

Non-exudative age-related macular degeneration, a prevalent cause of blindness, is a progressive and degenerative disease characterized by alterations in Bruch's membrane, retinal pigment epithelium, and photoreceptors exclusively localized in the macula. Although experimental murine models exist, the vast majority take a long time to develop retinal alterations and, in general, these alterations are ubiquitous, with many resulting from non-eye-specific genetic manipulations; additionally, most do not always reproduce the hallmarks of human age-related macular degeneration. Choroid vessels receive sympathetic innervation from the superior cervical ganglion, which, together with the parasympathetic system, regulates blood flow into the choroid. Choroid blood flow changes have been involved in age-related macular degeneration development and progression. At present, no experimental models take this factor into account. The aim of this work was to analyze the effect of superior cervical gangliectomy (also known as ganglionectomy) on the choroid, Bruch's membrane, retinal pigment epithelium and retina. Adult male C57BL/6J mice underwent unilateral superior cervical gangliectomy and a contralateral sham procedure. Although superior cervical gangliectomy induced ubiquitous choroid and choriocapillaris changes, it induced Bruch's membrane thickening, loss of retinal pigment epithelium melanin content and retinoid isomerohydrolase, the appearance of drusen-like deposits, and retinal pigment epithelium and photoreceptor atrophy, exclusively localized in the temporal side. Moreover, superior cervical gangliectomy provoked a localized increase in retinal pigment epithelium and photoreceptor apoptosis, and a decline in photoreceptor electroretinographic function. Therefore, superior cervical gangliectomy recapitulated the main features of human non-exudative age-related macular degeneration, and could become a new experimental model of dry age-related macular degeneration, and a useful platform for developing new therapies.

Published
2018
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39. A novel viewpoint in glaucoma therapeutics: enriched environment.

Author

González Fleitas MF, Dorfman D, and Rosenstein RE

Abstract

Glaucoma is one of the world's most frequent visual impairment causes and leads to selective damage to retinal ganglion cells and their axons. Despite glaucoma's most accepted risk factor is increased intraocular pressure (IOP), the mechanisms behind the disease have not been fully elucidated. To date, IOP lowering remains the gold standard; however, glaucoma patients may still lose vision regardless of effective IOP management. Therefore, the exclusive IOP control apparently is not enough to stop the disease progression, and developing new resources to protect the retina and optic nerve against glaucoma is a goal of vast clinical importance. Besides pharmacological treatments, environmental conditions have been shown to prevent neurodegeneration in the central nervous system. In this review, we discuss current concepts on key pathogenic mechanisms involved in glaucoma, the effect of enriched environment on these mechanisms in different experimental models, as well as recent evidence supporting the preventive and therapeutic effect of enriched environment exposure against experimental glaucomatous damage. Finally, we postulate that stimulating vision may become a non-invasive and rehabilitative therapy that could be eventually translated to the human disease, preventing glaucoma-induced terrible sequelae resulting in permanent visual disability., Competing Interests: None

Published
2022
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