Abstract
Commentary: Maternal immune activation evoked by polyinosinic: polycytidylic acid does not evoke microglial cell activation in the embryo.
Highlights
Immune-related abnormalities, which probably result from maternal infections during pregnancy, can be found in patients with schizophrenia and other mental disorders
In an elegant set of in vivo and in vitro experiments Smolders et al (2015) examined the effect of LPS and polyribocytidilic acid (poly I):C under identical conditions. They investigated whether embryonic microglia can be directly activated by incubating mouse brain slices from embryonic day 15.5 with either saline, poly I:C, IL-6, or LPS
When discussing possible pathophysiologic consequences of poly I:C’s failure to activate microglia, Smolders et al (2015) come to three conclusions: (i) It is unlikely that embryonic microglia dysfunction is the main mechanism that induces developmental abnormalities, (ii) poly I:C might evoke developmental deficits by directly acting on neuronal development, and Maternal Immune Activation and Embryonal Microglia (iii) it cannot be excluded that poly I:C effectuates an embryonic microglia priming, which results in an exaggerated response of microglia
Summary
Immune-related abnormalities, which probably result from maternal infections during pregnancy, can be found in patients with schizophrenia and other mental disorders. In the endeavor to simulate this environmental schizophrenia risk in animal models, maternal immune activation (MIA) by infectious agents has been introduced (Zuckerman et al, 2003; Meyer et al, 2005).
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