Abstract
A large number of studies indicate the role of early-life experience, in particular neonatal infections, in the formation of a high level of anxiety later in life. Changes in NMDA and AMPA glutamate receptor subunit composition that result in the violation of receptor functional activity may comprise the mechanism behind the behavioral impairments. Our work aimed to investigate exploratory and anxiety-like forms of behavior of adult rats that were treated with lipopolysaccharide (LPS) during the 3rd week of postnatal development at neuroinflammation-inducing doses. Levels of gene expression of NMDA receptor subunits (Grin1, Grin2a, Grin2b) and AMPA receptor subunits (Gria1, Gria2) in the medial prefrontal cortex, ventral and dorsal areas of the hippocampus were assessed by qRT-PCR. Our study on Wistar male rats revealed that the administration of LPS at doses of 25 and 50 μg/kg on P15, P18, P21 increased the expression of proinflammatory cytokine mRNA (interleukin-1β and tumor necrosis factor) in the hippocampus 2 h post treatment. Elevated expression of Grin2b, Gria1, Gria2 genes in the ventral hippocampus was observed 3 months after the administration of 50 μg/kg LPS compared with saline-treated control rats. Gria2 gene expression was found to be increased in the dorsal hippocampus 3 months after 25 μg/kg LPS injections in comparison with the controls. These changes were accompanied by impaired exploratory behavior of adult LPS-treated rats in the Open field test and a decreased level of anxiety in the Elevated plus maze. Taken together, our results substantiate early-life inflammation as a cause of prolonged changes in the hippocampal expression of genes of NMDA and AMPA receptor subunits and have an impact on related forms of behavior.
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