Browsing by Subject "RGC"

Now showing 1 - 3 of 3
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    Brain derived neurotrophic factor maintains Brn3a expression in axotomized rat retinal ganglion cells
    (Elsevier, 2009-08-16) Sánchez Migallón, María del Cielo; Nadal-Nicolás, Francisco Manuel; Jiménez López, Manuel; Sobrado Calvo, Paloma; Vidal Sanz, Manuel; Agudo Barriuso, Marta; Oftalmología, Optometría, Otorrinolaringología y Anatomía Patológica; Facultades de la UMU::Facultad de Medicina
    The transcription factor Brn3a has been reported to be a good marker for adult rat retinal ganglion cells in control and injured retinas. However, it is still unclear if Brn3a expression declines progressively by the injury itself or otherwise its expression is maintained in retinal ganglion cells that, though being injured, are still alive, as might occur when assessing neuroprotective therapies. Therefore, we have automatically quantified the whole population of surviving Brn3a positive retinal ganglion cells in retinas subjected to intraorbital optic nerve transection and treated with either brain derived neurotrophic factor or vehicle. Brain derived neurotrophic factor is known to delay retinal ganglion cell death after axotomy. Thus, comparison of both groups would inform of the suitability of Brn3a as a retinal ganglion cell marker when testing neuroprotective molecules. As internal control, retinal ganglion cells were, as well, identified in all retinas by retrogradely tracing them with fluorogold. Our data show that at all the analyzed times post-lesion, the numbers of Brn3a positive retinal ganglion cells and of fluorogold positive retinal ganglion cells are significantly higher in the brain derived neurotrophic factor-treated retinas compared to the vehicle-treated ones. Moreover, detailed isodensity maps of the surviving Brn3a positive retinal ganglion cells show that a single injection of brain derived neurotrophic factor protects retinal ganglion cells throughout the entire retina. In conclusion, Brn3a is a reliable retinal ganglion cell marker that can be used to accurately measure the potential effect of a given neuroprotective therapy.
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    Pan-retinal ganglion cell markers in mice, rats, and rhesus macaques
    (Kunming Institute of Zoology; the Chinese Academy of Sciences; and the China Zoological Society, 2022-12-16) Nadal-Nicolás, Francisco Manuel; Galindo Romero, Caridad; Lucas Ruiz, Fernando; Marsh-Amstrong, Nicholas; Li, Wei; Vidal Sanz, Manuel; Agudo Barriuso, Marta; Oftalmología, Optometría, Otorrinolaringología y Anatomía Patológica; Facultad de Medicina
    Univocal identification of retinal ganglion cells (RGCs) is an essential prerequisite for studying their degeneration and neuroprotection. Before the advent of phenotypic markers, RGCs were normally identified using retrograde tracing of retinorecipient areas. This is an invasive technique, and its use is precluded in higher mammals such as monkeys. In the past decade, several RGC markers have been described. Here, we reviewed and analyzed the specificity of nine markers used to identify all or most RGCs, i.e., pan-RGC markers, in rats, mice, and macaques. The best markers in the three species in terms of specificity, proportion of RGCs labeled, and indicators of viability were BRN3A, expressed by vision-forming RGCs, and RBPMS, expressed by vision- and non-vision-forming RGCs. NEUN, often used to identify RGCs, was expressed by non-RGCs in the ganglion cell layer, and therefore was not RGC-specific. γ-SYN, TUJ1, and NF-L labeled the RGC axons, which impaired the detection of their somas in the central retina but would be good for studying RGC morphology. In rats, TUJ1 and NF-L were also expressed by non-RGCs. BM88, ERRβ, and PGP9.5 are rarely used as markers, but they identified most RGCs in the rats and macaques and ERRβ in mice. However, PGP9.5 was also expressed by non-RGCs in rats and macaques and BM88 and ERRβ were not suitable markers of viability.
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    Visual deficits after traumatic brain injury
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Rasiah, Pratheepa Kumari; Geier, Ben; Jha, Kumar Abhiram; Gangaraju, Rajashekhar
    Traumatic brain injury (TBI) is frequently described as any head injury ceasing the brain's normal function. Anatomically, developmentally, and physiologically, the eye is deemed as an extension of the brain. Vision in TBI is underrepresented, and the number of active clinical trials in this field are sparse. Frequently, visual problems are overlooked at the time of TBI, often resulting in progressive vision loss, lengthening, and impairing rehabilitation. TBI can be either penetrative or non-penetrative, associated with degeneration of neurons, apoptotic cell death, inflammation, microglial activation, hemorrhage associated with vascular dysfunction; however, precise animal modeling that mimics the extensive visual deficits of TBI pathology remain elusive. Recent works in both the diagnostics and therapeutics fields are starting to make substantial progress in the right direction. Discussion of current advancements in TBI animal models and the recent pathophysiological findings related to the neuro-glia-vascular unit (NVU) will help elucidate novel targets for potential lines of therapeutics. Only over the past decade have newer pharmaceutical and stem cell-based treatments begun to come to light. The potency for these new lines of TBI specific curatives will be discussed along with the review of current blast-induced TBI models, providing potential directions for future research.