. 2015 Apr 7;5(4):e541. doi: 10.1038/tp.2015.33

Table 1. Summary of the effects that prenatal exposure to serum, LPA and LPA₁ antagonist produced in adult female mice.

Schizophrenia-related deficits	Serum	LPA	LPA1 antagonist
PPI	↓	↓	↑
Induced hyperactivity	↑	—	↓
Anxiety	↑	↑	↓
Social interaction	↓	—	—
Dopaminergic alterations	↑	↑	↓
GABAergic alterations	↓	±a	—a
Glutamatergic alterations	↓	↓	NA

Abbreviations: LPA, lysophosphatidic acid; NA, not assessed; PPI, prepulse inhibition; PV+, parvalbumin-positive.

Prenatal serum exposure induces several schizophrenia-related behavioral and neurochemical deficits that are primarily dependent on LPA receptor signaling. These models display good face validity (through validated schizophrenia-like deficits) and construct validity (through the modeling of prenatal hemorrhaging, a validated schizophrenia risk factor).

PV+ cell numbers were not decreased in prenatal LPA-exposed females. However, the expression of many GABAergic-related genes was altered in the PFC and midbrain of female mice prenatally exposed to LPA.

Table 1. Summary of the effects that prenatal exposure to serum, LPA and LPA1 antagonist produced in adult female mice.

Table 1. Summary of the effects that prenatal exposure to serum, LPA and LPA₁ antagonist produced in adult female mice.