Placental complications resulting in fetal growth restriction have been associated with dysregulated placental gene expression tied to an increased risk of schizophrenia. In rat offspring, it has been demonstrated that ∆9-tetrahydrocannabinol exposure in pregnancy results in fetal growth restriction and schizophrenia-like phenotypes (e.g., decreased pre-pulse inhibition of the acoustic startle response). However, it remains elusive if prenatal ∆9-tetrahydrocannabinol exposure induces this schizophrenia signature of placental gene expression. Therefore, our objective was to determine if these established predictive markers of schizophrenia are altered in a preclinical model of gestational oral ∆9-tetrahydrocannabinol exposure in rodents. We observed significantly reduced fetal weights in male and female prenatal ∆9-tetrahydrocannabinol-exposed offspring in the absence of maternal pregnancy outcomes. Placentae from ∆9-tetrahydrocannabinol-exposed males and females revealed altered expression of genes previously identified in human transcriptomic datasets of schizophrenia (i.e., Furin, Rccd1, and Atp5mk), with some expression changes being sex-specific (i.e., Eif5, Rps10, Vps33b, and Iqgap1). A subset of these genes were found differentially expressed in human BeWo cells exposed to ∆9-tetrahydrocannabinol. Targets were next examined in the adult rodent (postnatal day70) brain, and a subgroup of these genes (i.e., Furin, Rps10, and Rccd1) were increased concomitant with schizophrenia-like behavior (e.g., decreased pre-pulse inhibition). We further detected ∆9-tetrahydrocannabinol-induced upregulation of FURIN in patient-derived cerebral organoids, an effect observed in both control and schizophrenia cell lines. Collectively, these findings demonstrate prenatal ∆9-tetrahydrocannabinol exposure can lead to altered gene expression in established prioritized markers of schizophrenia in the placenta in both animal and human models.
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