Infection during pregnancy can lead to maternal inflammation. Several studies have suggested that maternal inflammation increases the risk on neuropsychiatric disorders, like autism, in the offspring. The cause of autism remains unknown. Vargas et al. demonstrated the presence of an active neuroinflammatory process in the brains of autistic patients, with marked microglial cell activation. Microglia colonize the central nervous system early in embryonic development, at the moment that neuronal migration to the cortical plate is peaking and neuronal differentiation and synaptogenesis are underway. By their production of growth factors, it has been suggested that microglia can influence axonal growth and synaptogenesis. The aim of this study is to determine the localization, activation stages and migration routes of the microglia present in the embryonic murine neocortex, in healthy embryos and embryos subjected to maternal inflammation. In the control group, as expected, the cell density and number of microglial ramifications increase as the embryo ages. This increase in cell density is also present in the inflammation group, however compared to the control it is more pronounced. Based on the expression levels of CD68 and CD11b, the microglial cells of the embryos subjected to maternal inflammation show a higher activation profile. The orientation of the protruding ramifications of microglia present in the parenchyma suggests that the cells migrate along radial glial fibers to reach their final position. Confocal images confirm contact between both cell types.