Modificaciones inducidas por la asfixia perinatal en el cerebelo de rata : neuroprotección por estrógeno
Perinatal asphyxia (AP) (1-5000 incidence live births) is an obstetric complication associated with a high rate of morbidity and mortality. The knowledge of the mechanisms involved in the disturbances caused by AP will allow the design of preventive or palliative therapies. The rapidly growing neona...
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| Formato: | Tesis de maestría acceptedVersion |
| Lenguaje: | Español |
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Facultad de Farmacia y Bioquímica
2015
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| Acceso en línea: | http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=afamaster&cl=CL1&d=HWA_1146 http://repositoriouba.sisbi.uba.ar/gsdl/collect/afamaster/index/assoc/HWA_1146.dir/1146.PDF |
| Aporte de: |
| Sumario: | Perinatal asphyxia (AP) (1-5000 incidence live births) is an obstetric complication associated with a high rate of morbidity and mortality. The knowledge of the mechanisms involved in the disturbances caused by AP will allow the design of preventive or palliative therapies. The rapidly growing neonatal cerebellum is vulnerable to hypoxia and may suffer functional alterations, including motor, cognitive and affective processes. We previously characterized hippocampal alterations using a murine model of AP; however, cerebellar alterations have not been completely described. Therefore, we studied morphological cerebellar alterations in adult rats (120 days old, 10-12 per group) suffering AP, and a later Estradiol (E2) treatment as a possible neuroprotective therapy. Sagittal sections of cerebellar lobes were analyzed by immunohistochemistry. The total number of Purkinje cells (PCs) remained constant in AP animals, but showed a higher percentage of abnormal cells with both calbindin toluidine blue staining. Purkinje cell layer exhibited a isorganized spatial configuration with PC clusters in some regions and gaps in others. At molecular layer level, an increased thickness was etected in asphyctic animals, together with the presence of edema in their dendrites, evidenced by an increased percentage of MAP2-reactive area. With respect to the granular layer, an increment in thickness was also observed in AP animals. In turn, an increase in reactive gliosis in both the granular and molecular layers (Bergmann glia and astrocytes, respectively) was observed in cerebella of AP animals, evidenced by an increased percentage of GFAP+ area and confirmed by Western blot. Finally, E2 treatment did not significantly improve alterations in AP animals. In conclusion, this study shows the long-term effects of AP in the cerebellar structure, which could\nbe involved in the pathogenesis of cognitive deficits observed in animals and 8 humans. E2 treatment failed to reverse changes produced by AP in rats, probably because of the type of estrogen receptor expressed in the cerebellum and the time analyzed. |
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