Cortical neural circuits are complex but very precise networks of balanced excitation and
inhibition. Yet, the molecular and cellular mechanisms that form the balance are just
beginning to emerge. Here, using conditional γ-aminobutyric acid receptor B1- deficient mice
we identify a γ-aminobutyric acid/tumor necrosis factor superfamily member 12-mediated
bidirectional communication pathway between parvalbumin-positive fast spiking interneurons and oligodendrocyte precursor cells that determines the density and function of
interneurons in the developing medial prefrontal cortex. Interruption of the GABAergic signaling to oligodendrocyte precursor cells results in reduced myelination and hypoactivity of
interneurons, strong changes of cortical network activities and impaired social cognitive
behavior. In conclusion, glial transmitter receptors are pivotal elements in finetuning distinct
brain functions
