Epilepsy is one of the most prevalent serious chronic neurological conditions worldwide. The World Health Organization (WHO) estimates 45-50 cases in 100,000 habitants in developed countries, rising to 122 to 190, in developing countries, including Brazil. There are no risk factors in relation to gender, race or age, but it is believed that some gene mutations are associated with an increased risk to develop the disease. The pathophysiology of epilepsy involves complex factors such as loss inhibition and increased neuronal excitability in different brain regions, but mainly at the hippocampus. Mutations in ion channels and in both receptor and neurotransmitter transporters may underlie disease pathogenesis. The inflammatory response plays an important role on epilepsy pathophysiology. Recent experimental evidence suggests a major role for both microglia and astrocyte activation on the seizure exacerbation. In this dissertation, we describe the general patterns of microgial and astrocyte activation and neuronal loss in CA1, CA3, hippocampal hylus, peririnal, lateral entorrinal and motor cortices and amigdaloid complex in the first week following “Status Epilepticus” induced by pilocarpine injection. Immunohistochemistry was performed to label neurons (anti-NeuN), microglia in general (anti-Iba1), activated microglia/macrophages (anti-ED1) and astrocytes (anti-GFAP). Numbers of neurons and activated microglia were counted in the hippocampus. There was intense microglia and astrocyte activation in all motor and limbic regions studied, mainly at 3 and 7 days post SE. Minocycline treatment reduced microglia activation in the hippocampus (p<0.05), without affecting astrocytosis. There was considerable inflammation in regions outside the hippocampus with an early inflammatory response. There was no neuronal loss in the hippocampus in the first week following SE, although sporadic alterations on neuronal morphology have been observed. These results suggest that the inflammatory response is an early and generalized histopathological event in several motor and limbic structures following pilocarpine-induced SE, even in the absence of conspicuous cell loss. The patterns of microglia and astrocyte activation can be used as markers of the progressive tissue impairment in the experimental models of epilepsy.
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