Patterns of proliferation and changes in total cell number in the optic nerve, tract and tectum of goldfish have been examined following optic nerve crush or optic enucleation, using bromodeoxyuridine to label the proliferating cells. In general, an increase in proliferation and total cell number in all parts of the visual system was observed peaking between 7 and 14 days and resolving itself to normal or near normal levels by 32 days postoperative. Enucleation resulted in elevated proliferation values as compared to animals with an optic nerve crush, at least one early timepoint in each part of the visual system, but overall, there is little to suggest that axons are exerting a major effect on the cellular response. Finally, a seasonal effect on the proliferative response of non-neuronal cells and axonal regrowth has been demonstrated. Fish acclimatized under autumn-like conditions showed a faster initiation of the non-neuronal cell response and an enhanced rate of axonal regrowth when compared to fish acclimatized under spring-like conditions. It is believed that photoperiod plays a major role in the seasonal effects observed with temperature playing only a minor one.

Background: Cryptococcal induced visual loss is common and increasingly becoming a debilitating consequence in survivors of cryptococcal meningitis (CM). Conflicting reports of the optic neuritis and papilloedema models of visual loss have delayed the introduction of effective interventional strategies for prevention and treatment of visual loss in CM. Qualitative and quantitative diffusion-weighted imaging (DWI) and diffusion tensor imaging (DTI) of the optic nerves have proven useful in the examination of the microstructure of the optic nerve especially in optic neuritis. Its application has been extrapolated to other optic nerve disorders such as ischaemic optic neuropathy and glaucoma. The aim of this study is to elucidate the pathogenesis of cryptococcal-induced visual loss using diffusion imaging of the optic nerve as an investigational tool. Method: Full ethical approval was obtained from the Greys Hospital, Department of Health and University of KwaZulu Natal Ethics Committees. Reliable and reproducible optic nerve diffusion techniques were first developed and optimized on 29 healthy volunteers at Greys Hospital, Neurology and Radiology departments using a Philips 1.5 Tesla Gyroscan. Informed consent was also obtained from 95 patients suffering from CM (≥18 yrs. of age), 14 patients with papilloedema and 14 patients with optic neuritis from other causes, recruited from Greys and Edendale Hospitals. Patients underwent full neuro-ophthalmological assessments, CSF examination, haematological workup, CD4 count, (viral load for some), electrophysiological assessment of vision [Visual evoked potential (VEP) and Humphreys visual fields (HVF)], Magnetic Resonance Imaging (MRI) scan of the brain and orbits and DWI and DTI of the optic nerves. Results and Discussion: Visual loss is common in CM, occurring in 34.6-48%. Optic neuritis was uncommon as evidenced by a lack of signal change and lack of enhancement within the optic nerve in all patients scanned. The peri-optic CSF space was not dilated and the optic nerve diameter was not increased regardless of CSF pressure and visual status. Swollen optic discs occurred in only 25% of patients whereas raised intracranial pressure (> 20cmCSF) was demonstrated in 69-71% of patients. Therefore visual loss could not be explained by papilloedema alone. The VEP P100 latency was shown to be a useful screening test for subclinical optic nerve disease in CM, but HVF was not. The optic nerve diffusion imaging used was reliable and reproducible and produced diffusion parameters equivalent to other investigators in the field. Neither optic nerve movement nor the CSF signal was demonstrated to impact significantly on optic nerve diffusion parameters. Optic nerve diffusion imaging did not demonstrate similarities between CM and papilloedema or optic neuritis regardless of CSF pressure or vision. Conclusion: The rarity of optic neuritis in CM and the disparity between papilloedema and visual loss together with the lack of support from diffusion studies suggest a 3rd mechanism of visual loss viz. the optic nerve compartment syndrome. Good clinical support is provided by a case report for this hypothesis that shows re-opening of the peri-optic CSF space and return of the peri-optic CSF signal on MRI with lowering of intracranial pressure and antifungal treatment. / Thesis (Ph.D.)-University of KwaZulu-Natal, Durban, 2013.

This study aims at providing a new technique for the isolation and culture of goldfish microglial cells. So far no protocol has been designed for the growth of these cells in vitro, despite the growing interest in the remarkable capacity of goldfish central nervous system (CNS) for regenerating severed axons. This newly developed technique has little or no similarity to those used in the isolation of mammalian microglia, and is distinguished by its simple setup and its fast yield for microglial cells. In addition, a virtually pure population of microglia was generated when plated on untreated plastic dishes, eliminating further need for purification. This technique may thus provide a starting point for future characterization of the microglial cells in vitro, which may eventually help toward building a better understanding of the function and biology of these cells. A preliminary morphological characterization of the cells has also been conducted, in addition to groundwork experiments on the phagocytic activity of these cells in vitro, using myelin to stimulate phagocytosis. These assays were oriented toward providing a comparison to the mammalian cultures of microglia, and so far, displayed several similarities in morphologies and phagocytosis.

Glaucoma is a common cause of blindness worldwide, yet the etiology of the disease is unclear. A leading hypothesis is that elevated intraocular pressure (IOP) affects the biomechanical environment within the tissues of the optic nerve head (ONH), and that the altered biomechanical environment contributes to optic nerve damage and consequent loss of vision. The biomechanical environment of the ONH is strongly dependent on the biomechanical properties of sclera, particularly scleral stiffness. However there is significant variability in reported stiffness data for human sclera. Therefore, our research goal was to measure the stiffness of human sclera and incorporate this information into finite element models of the human eye to characterize and quantify the biomechanical environment within and around the optic nerve head region at different IOP levels. Human sclera adjacent to the optic nerve head showed highly nonlinear, nearly isotropic and heterogeneous stiffness which was found to be substantially lower than that previously assumed, particularly at lower levels of IOP. The products c*c1 and c*c2, measures of stiffness in the latitudinal and longitudinal directions from the Fung constitutive model, were 2.9 ± 2.0 MPa and 2.8 ± 1.9 MPa, respectively, and were not significantly different (two-sided t-test; p = 0.795). Scleral stiffness was not statistically different between left and right eyes of an individual (p = 0.952) and amongst the quadrants of an eye (p = 0.412 and p = 0.456 in latitudinal and longitudinal directions, respectively). Three stress-strain relationships consistent with the 5th, 50th and 95th percentiles of the measured scleral stiffness distribution were selected as representatives of compliant, median and stiff scleral properties and were implemented in a generic finite element model of the eye using a hyperelastic five-parameter Mooney-Rivlin material model. Models were solved for IOPs of 15, 25 and 50 mmHg. The magnitudes of strains at the optic nerve head region were substantial at even the lowest applied IOP (15 mmHg) and increased at elevated IOPs (e.g. the third principal strain in the compliant model reached as much as 5.25% in the lamina cribrosa at 15mmHg and 8.84% in the lamina cribrosa at 50 mmHg). Scleras that are “weak”, but still within the physiologic range, are predicted to lead to appreciably increased optic nerve head strains and could represent a risk factor for glaucomatous optic neuropathy. As IOP increased from 15 to 50 mmHg, principal strains in the model with a compliant sclera increased at a lower rate than in the model with a stiff sclera. We quantified the biomechanical environment within and around the optic nerve head region using a range of experimentally measured mechanical properties of sclera and at different IOPs. We showed that IOP-related strains within optic nerve head tissues can reach potentially biologically significant levels (capable of inducing a range of effects in glial cells) even at average levels of IOP and for typical human scleral biomechanical properties.

No description available.

Thesis (Ph. D.)--University of Hong Kong, 1998. / Includes bibliographical references (leaf 119-140).

Thesis (Ph.D.)--University of Western Australia, 2007.

Vários trabalhos têm mostrado que a ingestão deficiente de ferro pode causar alterações nos parâmetros morfológicos e bioquímicos do Sistema Nervoso Central (SNC) do rato assim como em seu comportamento. Também, os animais deficientes em ferro mostram redução no número de lamelas de mielina e déficits de aprendizado. Por outro lado, a estimulação tátil pode reduzir e/ou evitar os danos causados pela má nutrição sobre o SNC e comportamento. Entretanto, os danos no processo de mielinização têm também sido vistos na anemia ferro-deficiente e, uma vez que o nervo óptico é em grande parte formado pelos axônios mielinizados, o objetivo deste estudo é verificar os efeitos da anemia ferropriva e estimulação tátil sobre a morfologia do nervo óptico de ratos Wistar machos aos 18, 22 e 32 dias de idade. Os animais foram divididos em 2 grupos: Controles ( C ) (35 mg Fe / Kg de dieta), Anêmicos ( A ) (4 mg Fe / Kg de dieta). Cada grupo foi subdividido em Estimulado ( E ) e Não Estimulado ( N ). O peso corporal, hemoglobina, hematócrito, área, perímetro, diâmetro mínimo, densidade de células gliais e número de vasos no nervo óptico foram avaliados. Os animais foram anestesiados com éter sulfúrico e sacrificados por perfusão cardíaca com PBS 0,05 M em pH 7,3, seguido por paraformaldeído 2% mais glutaraldeído 1% em tampão fosfato 0,1 M (pH 7,3). O nervo óptico foi dissecado e imerso em solução de tetróxido de ósmio a 1% por duas horas a 40C, desidratado em acetona com graus de diluição crescentes e incluído em araldite. As amostras de nervo óptico foram orientadas para permitir cortes transversos de suas fibras. Secções de 0,5 m foram obtidas e coradas com azul de toluidina 1% antes de serem examinadas na microscopia de luz. Os estudos morfométricos foram feitos com um sistema analisador de imagens semi-automático (MiniMop). Os resultados mostram que a anemia levou a deficiências no peso corporal, hematócrito, hemoglobina, área, perímetro, diâmetro mínimo, número de células gliais e número de vasos do nervo óptico entre os anêmicos, e que a estimulação melhorou significativamente estes itens tanto em anêmicos quanto em controles (à exceção de hematócrito e hemoglobina) porém não recuperando totalmente os estes prejuízos provocados pela anemia. / Several works have been shown that the deficient ingestion of iron can cause alterations in the morphologic and biochemical parameters of the Central Nervous System (CNS) of the rat as well as in its behavior. Also, the iron deficient animals show reduction in the number of myelin lamellae and learning deficits. On the other hand, the tactile stimulation can reduce and/or to avoid the damages caused by the bad nutrition about CNS and behavior. However, the damages in the myelinization process have been seen also in the iron-deficient anemia and, at once that the optical nerve is formed largely by the myelinated axons, the objective of this study is to verify the effects of the anemia and tactile stimulation on the morphology of the optical nerve of Wistar males rats at the 18th, 22 nd and 32 nd days of age. The animals were divided in 2 groups: Controls © (35 mg Fe / diet Kg), Anemic (A) (4 mg Fe / diet Kg). Each group was subdivided in Stimulated (S) and No Stimulated (N). The corporal weight, haemoglobin, haematocrit, area, perimeter, minimum diameter, density of glial cells and number of vases were evaluated. The animals were anesthetized and sacrificed by heart perfusion with PBS 0,05 M in pH 7,3, following for paraformaldheyde 2% plus glutaraldheyde 1% in a phosphate buffer 0,1 M (pH 7,3). The optic nerve was dissected and submerged in solution of osmium tetroxide 1% for two hours at 40C, dehydrated in acetone with decreasing dilution degrees and included in araldite. The samples of optic nerve were guided to allow transverse cuts of their fibers. Sections sized 0,5 m were obtained and stained with toluidin blue 1% prior examinations in the light microscopy. The morphometric studies were made with a semiautomatic analyzing system of images (MiniMop). The results show that the anaemia caused differences in the corporal weight, haematocrit, haemoglobin, area, perimeter, minimum diameter, number of glial cells and vassels of the optical nerve among controls and anaemic, and that the stimulation influenced significantly on these items taking to the conclusion that it improves the damaged structures due to anaemia, but it doesn’t recover them totally.

Indiana University-Purdue University Indianapolis (IUPUI) / Hydrocephalus affects 1 in 1,000 newborns and nearly 1,000,000 Americans, leading to an increase in intercranial pressure due to the build-up of cerebrospinal fluid. There are numerous complications that arise as a result of hydrocephalus, but this study focuses on optic disc edema. The subarachnoid space surrounding the optic nerve contains cerebrospinal fluid. The cerebrospinal fluid increases in hydrocephalus, putting pressure on the optic nerve. The additional intracranial pressure has been proposed to cause axoplasmic stasis within the retinal ganglion cell axons, leading to axonal damage and retinal ischemia. The purpose of this study was to determine the effects of hydrocephalus on the optic disc and retina in several animal models of hydrocephalus. This study uses two genetic and two injury-induced models of hydrocephalus in addition to immunohistochemistry and histological stains to examine the optic disc, thickness of retinal layers, and numbers of retinal cells. This study serves as preliminary work to help build the case that hydrocephalus causes cell loss in the retina, as well as swelling of the retinal ganglion cell axons, leading to axoplasmic stasis and cell death. / Indefinitely

No description available.