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Interestingly, maternal inflammation has also been associated with a significant increase in glutaminase, an increase in NMDAR subunit GluN2 (NR2) expression and impairment of GLT-1 function, all things that trigger excitotoxicity.[284] Because of the interaction between GluRs and their subunits and inflammatory mediators, it is difficult to separate which component of immunoexcitotoxicity is actually playing the most important part in altering neural development and laminar architecture of the cortex
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