Browsing by Subject "Intraocular pressure"

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    Effects of a non-selective ß-blocker on adult rat anterograde axonal transport and retinal ganglion layer after increased intraocular pressure
    (Murcia : F. Hernández, 2005) Díaz, F.; Villena, A.; Moreno M.; Vidal, L.; Parrado, C.; García-Campos, J.; Perez de Vargas, I.
    The aim of this study was to examine the effects of timolol in an experimental model of elevated intraocular pressure (IOP). Three episcleral veins of rats with normal IOP were cauterized. Three months later we examined the effects on anterograde axonal transport from the retinal ganglion cells (RGCs) to the superior colliculus (SC) as well as on the number of neurons in the retinal ganglion layer (RGL). These parameters were also studied in a group of rats submitted to treatment with timolol after confirming that their IOP was still raised after two weeks. After the surgical procedure, the mean IOP of the experimental eyes increased to 33.5±1.06 mmHg (1.25 fold compared to the control group) and three months later the IOP remained significantly elevated; however, after a long period of treatment with timolol the IOP was 14.05±0.81 mmHg, similar to that of the control group. In the group with normal IOP, labelling with horseradish rabbit peroxidase (HRP) at 120 minutes and 24 hours postinjection showed continuous staining from the retina to the SC. In the experimental group the optic nerve head (ONH) was completely negative, although in the group treated with timolol there was partial block of axonal transport in the ONH, in which the staining was slightly more intense The number of neurons in the RGL, counted by immunohistochemical labelling with Neu-N, showed that in eyes with normal and elevated IOP there were 423±11 neurons/mm2 and 283±10 neurons/mm2, respectively. After treatment with timolol the number of neurons (331±10 cells/mm2) increased compared with elevated IOP eyes, although the number did not reach that of the control group. These results indicate that treatment with timolol, started two weeks after the surgical procedure, was partially neuroprotective because the loss of neurons in the RGL was lower than in untreated animals, though not sufficient to re-establish normal axonal transport.
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    Understanding glaucomatous damage: Anatomical and functional data from ocular hypertensive rodent retinas
    (Elsevier, 2012-01-27) Miralles de Imperial, Jaime; Vidal Sanz, Manuel; Salinas Navarro, Manuel Ángel; Nadal-Nicolás, Francisco Manuel; Valiente Soriano, Francisco Javier; Agudo Barriuso, Marta; Villegas Pérez, Maria Paz; Avilés Trigueros, Marcelino; Alarcón Martínez, Luis; Oftalmología, Optometría, Otorrinolaringología y Anatomía Patológica; Facultades de la UMU::Facultad de Medicina
    Glaucoma, the second most common cause of blindness, is characterized by a progressive loss of retinal ganglion cells and their axons, with a concomitant loss of the visual field. Although the exact pathogenesis of glaucoma is not completely understood, a critical risk factor is the elevation, above normal values, of the intraocular pressure. Consequently, deciphering the anatomical and functional changes occurring in the rodent retina as a result of ocular hypertension has potential value, as it may help elucidate the pathology of retinal ganglion cell degeneration induced by glaucoma in humans. This paper predominantly reviews the cumulative information from our laboratory’s previous, recent and ongoing studies, and discusses the deleterious anatomical and functional effects of ocular hypertension on retinal ganglion cells (RGCs) in adult rodents. In adult rats and mice, perilimbar and episcleral vein photocauterization induces ocular hypertension, which in turn results in devastating damage of the RGC population. In wide triangular sectors, preferentially located in the dorsal retina, RGCs lose their retrograde axonal transport, first by a functional impairment and after by mechanical causes. This axonal damageaffects up to 80% of the RGC population, and eventuallycauses their death, with somal and intraretinal axonal degeneration that resembles that observed after optic nerve crush. Importantly, while ocular hypertension affects the RGC population, it spares non-RGC neurons located in the ganglion cell layer of the retina. In addition, functional and morphological studies show permanent alterations of the inner and outer retinal layers, indicating that further to a crush-like injury of axon bundles in the optic nerve head there may by additional insults to the retina, perhaps of ischemic nature.