We next examined whether neurodevelopmental defects from a synergistic interaction between stress and DISC1 KD also requires depolarizing GABA signaling during early postnatal neurogenesis. Expression of shRNA-NK1 completely suppressed DISC1 KD-induced dendritic growth following maternal deprivation stress (Figures 6C to 6D). Interestingly, co-expression of shRNA-NK1 also largely suppressed soma hypertrophy and ectopic primary dendrite formation from shRNA-D1 expression at 7 dpi (Figures S6B to S6C), whereas aberrant neuronal positioning was not rescued (Figure S6D). Furthermore, treatment of rapamycin rescued DISC1 KD-induced defects of newborn neurons during early postnatal neurogenesis after maternal deprivation (Figures 6E to 6F, S6E to S6H and Table S1), suggesting a conserved mechanism underlying DISC1-dependent regulation of neuronal development between early postnatal neurogenesis after stress and during normal adult neurogenesis.
