The prefrontal cortex (PFC) is a pivotal brain region for cognitive functions, including working memory, planning, reasoning, and decision-making. Recent studies have identified abnormalities (e.g. deficient myelination, aberrant neurotransmission, excitatory/inhibitory imbalance) in the PFC of developmental psychiatric disorders, namely autism and schizophrenia, supporting an idea that dysregulation of the circuitry development in PFC may be involved in these disorders. Knowledge on how these processes proceeds during normal brain development is crucial to understand involvement of developmental dysregulation in pathogenesis of these disorders. To this end, we performed comprehensive quantitative polymerase chain reaction (qPCR) analysis using mouse brains. Expression of oligodendrocyte/myelin related genes (e.g. Cldn11, Plp1) and fast-spiking interneuron marker gene, Pvalb, were dramatically increased between postnatal days 7 (P7) and P21, and peaked at P21 and P35, respectively. On the other hand, there were little changes in genes for neurotransmitter receptors (dopamine, AMPA, and NMDA receptors), postsynaptic molecules, and cell adhesion molecules. These patterns are unique to PFC compared to any other brain regions. In addition, we characterized responsiveness to NMDA antagonist by measuring extracellular glutamate level in the PFC using in vivo microdialysis after a MK-801 administration. While basal extracellular glutamate level reached nearly equal adult level, MK-801 sensitivity was still high at P42, and then it was stabilized to adult level at P56. These results indicate that timing of circuit maturation may be around P42 or later in PFC. These basic data on normal development should help us to have better ideas on the events in normal and pathological situations taking place in PFC.