Background: Degenerative changes caused by aging may affect the eye, especially the retina. Such changes occur as a part of normal physiological process and may be irreversible. The aim of the study was to demonstrate the influence of aging on the morphology of the retina to provide a basis to explain the pathogenesis of age-associated decline in visual acuity, scotopic and photopic sensitivity. Materials and methods: Forty male albino rats were used and divided into four age groups (group I: age of cortical maturity, group II: middle-aged, group III: aged group and group IV: senile group). The rats were sacrificed, the eye balls were enucleated. Intra-vitreal injections of formalin for haematoxylin and eosin and immunohistochemical sections, glutaraldehyde for toluidine blue semithin and E/M ultra-thin sections were performed. Measurements and quantitative histomorphometric estimation of the layers of the retina were done. Results: Light microscopic examination revealed age-dependent attenuation of photoreceptor striations. Aged and senile groups presented pyknotic, widely-spaced nuclei of the outer nuclear layer. The inner nuclear layer was thinned out to 2 or 3 cellular rows. Retinal capillaries showed progressive dilatation and congestion. Statistical analysis proved significant thinning of the retina with variable degrees of thinning of the constituting layers. Decreased arborisation with age was confirmed with quantification of synaptophysin-immunostained sections. Glial fibrillary acidic protein immunostaining revealed the picture of reactive gliosis. On the ultrastructural level, the retinal pigment epithelium exhibited major alterations with aging. Numerous phagosomes, lipofuscin and melanolipofusin granules appeared within the cells, together with exaggerated basal infoldings. The photoreceptor nuclei became degenerated and the perinuclear space was widened. Conclusions: Rat retinae clearly undergo age-related morphological changes. Such changes provide a cellular base for explanation of decreased vision in humans with aging other than reflection errors. Effect of aging was not only qualitative, but also quantitative. (Folia Morphol 2019; 78, 2: 237–258)
Background: As the hippocampus is the main brain region for many forms of learning and memory functions and is acutely sensitive to blood glucose changes, diabetes mellitus, which is a serious metabolic disease, is often accompanied by learning and memory deficits. Through scientific literatures, mesenchymal stem cells (MSCs) promote functional recovery in rats with traumatic brain injury, so the present work was conducted to study MSCs as a possible treatment for the diabetic neuronal degeneration and functional impairment of rat hippocampus. Materials and methods: It was carried out using male albino rats: non-diabetic control groups (4, 8, 12 weeks) (n = 15), diabetic groups by i.v. injection of streptozotocin for (4, 8, 12 weeks) (n = 15) and MSCs treatment to diabetic groups for (8, 12 weeks) (n = 10). Hippocampal learning and memory functions were assessed by the Morris Water Maze test and its results were statistically analysed. The rat hippocampal regions (CA1 and CA3) were subjected to histological, ultrastructural examination and morphometrical analyse of pyramidal neurons. Results: Neurons of the diabetic groups showed disturbed function and architecture; shrunken hyperchromatic nuclei and vacuolated eosinophilic cytoplasm (apoptotic changes) also MSCs treatment improved hippocampal learning and memory functions plus its architectural changes; increasing populations and normal regular distribution. Conclusions: It can be concluded that diabetic hippocampal neuronal alternations and functional impairment can be ameliorated by MSCs treatment. (Folia Morphol 2020; 79, 2: 211–218)
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