Maternal immune activation (MIA) contributes to behavioral abnormalities relevant to schizophrenia in adult offspring, although the molecular mechanisms underlying MIA-induced behavioral changes remain unclear. Here we demonstrated that dietary intake of glucoraphanin (GF), the precursor of a natural antioxidant sulforaphane, during juvenile and adolescent stages prevented cognitive deficits and loss of parvalbumin (PV) immunoreactivity in the medial prefrontal cortex (mPFC) of adult offspring after MIA. Gene set enrichment analysis by RNA sequencing showed that MIA caused abnormal expression of centrosome-related genes in the PFC and hippocampus of adult offspring, and that dietary intake of GF improved these abnormal gene expressions. Particularly, MIA increased the expression of suppressor of fermentation-induced loss of stress resistance protein 1 (Sfi1) mRNA in the PFC and hippocampus of adult offspring, and dietary intake of GF prevented the expression of Sfi1 mRNA in these regions. Interestingly, we found altered expression of SFI1 in the postmortem brains and SFI1 mRNA in hair follicle cells from patients with schizophrenia compared with controls. Overall, these data suggest that centrosome-related genes may play a role in the onset of psychosis in offspring after MIA. Therefore, dietary intake of GF-rich vegetables in high-risk psychosis subjects may prevent the transition to psychosis in young adulthood.

This study suggests that SB induced antipsychotic effects in the PCP model of schizophrenia, although it did not increase D-serine levels in the brain.

The stabilization of chicken ovalbumin (OVA) mRNA by different classes of steroid hormones (estrogen, progesterone, glucocorticoid, and androgen) was studied in the oviducts of chicks treated with combinations of four steroids. The combination of estrogen with progesterone, glucocorticoid, or androgen enhanced the induction of the OVA gene more than did estrogen alone. Run-on analysis of the isolated oviduct nuclei to measure the transcription rate of the OVA gene showed that the enhanced induction of the OVA gene by the combined hormone treatments was partly caused by an increased rate of transcription. The half-life of OVA mRNA as determined using a transcription inhibitor (actinomycin D) was estimated to be about 24 h irrespective of the hormone treatment, though the half-life was about 6 h in the absence of hormones. These results suggested that the prolongation of the half-life of OVA mRNA by steroid hormones is constant irrespective of differential transcription rates of the OVA gene.

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