DRP004096
Intake of glucoraphanin during juvenile and adolescent stages prevents cognitive deficits in adult offspring after maternal immune activation: Role of centrosome
Prenatal infection and subsequent abnormal neurodevelopment of offspring is involved in the etiology of schizophrenia; which is associated with oxidative stress. Sulforaphane (SFN) is a natural compound with a potent anti-oxidant activity. This study was undertaken to examine whether dietary intake of glucoraphanin (GF), a precursor of SFN, can prevent the behavioral abnormalities in the offspring after maternal immune activation (MIA). The polyriboinosinic-polyribocytidilic acid [poly(I:C); 5.0 mg/kg/day from E12 to E17] or saline were injected into pregnant mice. Four-weeks old male offspring mice were divided into a normal food pellet group and a 0.1% GF containing pellet group during 4 weeks. Behavioral tests and parvalbumin (PV)-immunohistochemistry were performed at adult. Cognitive deficits and loss of PV-immunoreactivity in medial prefrontal cortex (mPFC) in the juvenile offspring after MIA were shown. Dietary intake of 0.1% GF from P28 to P56 significantly improved cognitive deficits and loss of PV-immunoreactivity in the mPFC of adult offspring after MIA.  The RNA-seq analysis showed that centrosome may play a role in the beneficial mechanisms of GF intake. In conclusion, this study suggests that dietary intake of GF during juvenile and adolescence stage could prevent cognitive deficits and PV-loss in the mPFC of adult offspring after MIA. Therefore, the dietary intake of SFN-rich foods in high-risk subjects for psychosis may prevent conversion to psychosis.