Fig. 2.

Emergence of Distinct Psychopathological and Neuropathological Symptom Clusters in Adulthood After Prenatal Polyriboinosinic-Polyribocytidilic Acid (PolyI:C)–Induced Immune Activation in Early/Middle (Red) and Late (Blue) Gestation in the Mouse. The diagram illustrates the identified structural and functional brain abnormalities that are characteristic of the symptom profiles associated with prenatal PolyI:C exposure in early/middle and late gestation. Some of the psychopathological and neuropathological traits are clearly restricted to the symptom cluster associated with prenatal immune activation in early/middle or late gestation, whereas others are common to both symptom clusters. The exact correspondence between the distinct neuropathological and psychopathological symptom clusters remains to be determined. The neuropathological effects presented in brackets denote that they were studied only after prenatal PolyI:C–induced immune activation in early/middle gestation so far. AMG, amygdala; AMPH, amphetamine; D1R/D2R, dopamine D1/D2 receptor; dHPC, dorsal hippocampus; GABA_A-R, gamma-amino-butyric acid (A) receptor; mPFC, medial prefrontal cortex; MK-801, dizocilpine; NAc, nucleus accumbens; PV, Parvalbumin; TH, tyrosine hydroxylase; US, unconditioned stimulus; vHPC, ventral hippocampus.