Polyunsaturated fatty acids (PUFAs) are essential for brain development and function. Increasing evidence has shown that an imbalance of PUFAs is associated with various human psychiatric disorders, including autism and schizophrenia. Fatty acid-binding proteins (FABPs), cellular chaperones of PUFAs, are involved in their intracellular trafficking, signal transduction, and gene transcription. Previously, we showed that FABP3 is strongly expressed in the parvalbumin (PV)-positive inhibitory interneurons (PV interneurons) of the adult mouse anterior cingulate cortex (ACC), which is a part of rodent medial prefrontal cortex (mPFC) and is important for the coordination of cognitive and emotional behaviors. Although the expression of FABP3 becomes evident after birth, the function of FABP3 is largely unknown in postnatal brain. In particular, the effects of FABP3 deletion in the ACC PV interneurons are unclear. In this study, we first confirmed that FABP3 was expressed in the PV interneurons of postnatal day 14 (P14) ACC. PV synapse density increased in the P14 ACC of Fabp3 KO mice, whereas the number of PV interneurons remained unchanged. These results suggest that FABP3 is involved in the formation of inhibitory synapse in the ACC.