Background

Epidemiological studies provide substantial evidence for an association between prenatal infections and increased risk for the development of some neuropsychiatric disorders, such as schizophrenia and autism, in the offspring (Brown and Meyer, 2018). Indeed, inflammation in pregnancy may alter normal development of the fetus thereby increasing the risk of the emergence of psychopathologies. Accurate identification of the mechanisms underlying these effects may advise early interventions. As a result, a number of research groups have developed models of MIA in rodents and non-human primates that offer a fruitful opportunity to examine the complex etiology of complex psychiatric disorders. Researchers have used these models to assess behavioural, pharmacological, and pathophysiological outcomes of MIA in the offspring (for reviews of this literature, see: Piontkewitz et al., 2012; Reisinger et al., 2015; Estes and McAllister, 2016; Careaga et al., 2017; Brown and Meyer, 2018; Bergdolt and Dunaevsky, 2019; Gumusoglu and Stevens, 2019; Kentner et al., 2019; Meyer, 2019). The protocol we describe below is adapted from Lins et al. (2018 and 2019) with some changes including our protocol for in-house timed pregnant breeding of rats. The use of a viral mimetic instead of infection with a virus is advantageous as the duration of the effect is better controlled and biosafety concerns are reduced. Some studies have shown similar effects on the offspring following inoculation of pregnant mice with the influenza virus thereby supporting the validity of the polyI:C model (Shi et al., 2003).