(1) In utero exposure to EMIP induced persistent neurocognitive deficit and affective disorders in the offspring. (2) In utero EMIP-induced cognitive deficit in offspring was rescued by genetic or pharmacological disruption of C5aR signaling. (3) In utero EMIP-induced reduction in neurotransmitter levels (dopamine, 5-HT, and norepinephrine) was observed only in WT (not in C5aR deficient) offspring. Here, C5AR1 is linked to Cognitive impairment.