Figure 2.
Genetic predisposition would heighten stress responsivity during adolescence. Extreme stress exposure leads to parvalbumin (PV) loss in the ventral subiculum (vSub) of hippocampus, which can be a consequence of enhanced oxidative stress. This PV loss contributes to the vSub hyperactivity and, consequently, alterations in vSub output (via nucleus accumbens and ventral pallidum; NAc-VP) that drives a hyper-responsive dopamine (DA) system in the ventral tegmental area (VTA) that underlies the emergence of psychosis at late adolescence/early adulthood. Thus, early interventions using stress management and antioxidants would be useful to prevent the transition into schizophrenia, while antipsychotics are effective at onset of psychosis.