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HERNANDES, M. S. Reactive oxygen species generation and neuroinflammation induced by ocular enucleation in the rat visual system. 2011. 155 p. Ph.D. Thesis (Human Physiology) – Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, 2011. Unilateral ocular enucleation represents a useful model to study visual system plasticity. In the first part of this thesis, we evaluated the reactive oxygen species (ROS) generation in the main visual relays of the mammalian brain, namely the superior colliculus (SC) and the dorsal lateral geniculate nucleus (DLG), after ocular enucleation. Dihydroethidium oxidation revealed increased ROS generation in SC and DLG. ROS generation was decreased by the Nox inhibitors DPI and apocynin. Real-time PCR results revealed that Nox 2 was upregulated in both retinorecipient structures after deafferentation, whereas Nox 1 and Nox 4 were upregulated only in the SC. To evaluate the role of ROS in structural remodeling after the lesions, apocynin was given to enucleated rats and immunohistochemistry was conducted for markers of neuronal remodeling into SC and DLG. Immunohistochemical data showed that ocular enucleation produces an increase of neurofilament and microtubule-associated protein-2 immunostaining in both SC and DLG, which was markedly attenuated by apocynin treatment. In the second part of the study, we focused on the hypothesis that the deafferentation of visual system may generate inflammatory-mediated responses in the SC. We first observed that glial cells protein expression is markedly increased after the lesion. Electrophoretic mobility shift assays (EMSA) to detect nuclear factor B (NFB) activation indicated that this transcription factor is activated in the SC from 1 hour to day 15 after the lesion. These periods approximately coincided with the increased expression of cyclooxygenase-2, which is a target gene for NFB. To evaluate the role of an anti-inflammatory drug in attenuating both NFB and glial cells activation, the glucocorticoid dexamethasone (DEX) was administered (1mg/kg i.p., for 3 days) to enucleated rats and immunohistochemistry was performed to detect markers of astrocytes and microglia activation. The immunostaining revealed increased astrocyte and microglia proliferation after the lesion, which was significantly reduced by the DEX treatment. Similarly, NFB activation was attenuated by DEX treatment. Taken together, the findings of the present study suggest a novel role for Nox-induced ROS signaling in mediating neuronal remodeling in visual areas after ocular enucleation. Moreover, these results raise the possibility that the removal of retinal ganglion cell input generates inflammatory responses in the SC.

Geração de espécies reativas de oxigênio e neuroinflamação induzidas por enucleação ocular no sistema visual de ratos.