Objective The cortical barrel is an ideal model for the study of experience-depend conical development and plasticity.Abnormal plasticities have been detected in the cortical barrels in many animal disease models.However, the mechanisms underlying barrel development remain to be elucidated.Methods In this study, we first examined cortical neuron differentiation and thalamocortical afferents (TCA) branches in primary somatosensory cortex in detail after unilateral infraorbital nerve transaction (ION) at P2, and then detected the gene expressions.The transcription factor forkhead box G1 (FoxG1) was found to be down-regulated remarkably.To elucidate the function of FoxG1 in postnatal cortical barrel development, a FoxGlflox/flox mouse line was crossed with CAG-CreERTM and FoxG 1 was conditionally disrupted at specific stages when is critical for cortical barrel development.Results After ION at P2, TCA could not segregate properly to form cortical barrel hollow, and the normal distribution patterns of CR+ and PV+ interneuron within the cortical barrels were disrupted.Meanwhile, the protein level of NeuroD2, Tbr1, Cux1 and Foxp2 were reduced, indicating the maturation of pyramidal cells was affected.Furthermore, a remarkable down-regulation of FoxG1 was observed after ION suggesting important functions of FoxG 1 in cortical barrel development.When FoxG1 was conditionally inactivated at E14.5, the number of Cux1+ neurons in upper cortical layer was remarkably reduced, instead the number of Ctip2+ neurons in deep layer increased.CR+ interneuron and TCA terminals were ectopically located in the ventricular zone (VZ) while normally they should be located above the VZ.When FoxG 1 disrupted at P2, the number of CR+ interneuron increased, the number of Cux1 +neurons decreased further, with Ctip2+ neurons dispersed.This led to the wall of cortical barrels was hardly to be seen at P10.Conclusion FoxG1 is critical for the cortical barrel development.