During the early postnatal period in mice, multiple critical processes are underway including axonal elaboration and synaptogenesis, as well as structural reorganization of the developing neocortex such as cortical plate positioning. Interestingly, NRG3 expression is enriched in the cortical antihem during late embryogenesis, where it is thought to be important in the regulation of cortical patterning. Therefore, it is possible that transient overexposure to NRG3 during early postnatal life disrupts cortical circuit DAPT development which is critical for normal mature brain function. Other neurodevelopmental models studying early developmental factors that may increase predisposition to schizophrenia have highlighted the importance of the neonatal period in the pathogenesis of schizophrenia and other neuropsychiatric disorders including the neonatal lesion model in rodents and non-human primates which elicit a broad spectrum of schizophrenia related behavioral phenotypes. Finally, although further work is needed to determine the biological role of NRG3 at differing critical periods of development, the current study bridges a gap in understanding the pathophysiological role of NRG3 in neurodevelopmental disorders such as schizophrenia and autism, and provides a valuable rodent model system for study of developmental neurotrophin overexposure without need for genetic manipulation. Together, our data suggest that NRG3 plays a prominent role in early postnatal brain development where it potentially modulates the construction and plasticity of newly developing brain circuits relevant to anxiety and social cognition. Spinal dorsal horn neurons not only relay sensory information to higher brain centers, but also form neuronal circuits to process primary sensory information. Sensory stimulation-evoked neuronal activity of SDH projection neurons is modified by polysynaptic sensory inputs through interneurons. The fact that pharmacological inhibition and targeted disruption of SDH interneurons disturb somatic sensation indicates crucial roles of the SDH interneurons for neuronal processing of sensory information. The significance of SDH interneurons is also exemplified by allodynia or hyperalgesia, which are caused at least in part by dysfunction of or damage to these interneurons. SDH interneurons are also involved in the spatial tuning of the tactile and nociceptive systems. Previous electrophysiological and immunohistochemical studies have elucidated neuronal connectivity of SDH projection neurons and interneurons.