Maternal deprivation increases microglial activation and neuroinflammatory markers in the prefrontal cortex and hippocampus of infant rats.

A relationship between neuroinflammation and the development of psychiatric disorder have been revealed by many studies in the past decade. Although studies have shown that stressors can induce long-term changes that may be related to behavioral responses, these alterations have been poorly studied soon after a stressor, such as maternal deprivation (MD). Thus, this study was designed to investigate the acute effect of experimental induction of MD on inflammatory and microglial activation markers in the brain of infant rats. Early MD was induced from postnatal day (PND) 1-10. On PND 10 the prefrontal cortex (PFC) and hippocampus from MD and control groups were removed to investigate microglial activation and neuroinflammatory markers. In the PFC the expressions of cluster of differentiation molecule 11B (CD11B), toll-like receptor (TLR)-2, and TLR-4 were increased in rats subjected to MD. The arginase expression was elevated in the PFC and hippocampus of maternally deprived rats. The cytokines interleukin-5 (IL-5), -6, -7, -10, tumor necrosis factor (TNF-α), and interferon gamma (INF-γ) were increased in the PFC of MD rats group. In the PFC the macrophage inflammatory proteins (MIP)-1α levels were reduced in MD rats group. In the hippocampus only the levels of TNF-α and INF-γ were elevated in infant rats subjected to MD. In conclusion, our results support the hypothesis that neuroinflammation and microglial activation, mainly in the PFC, could be involved with changes in the brain resident cells following MD, and these alterations could be associated to the development of psychiatric conditions late in life.