Injury of sensory afferents causes large-scale somatotopic reorganization in the brain. However, mechanisms of neural circuit remodeling underlying the reorganization remain largely unclear. A relay neuron in the mouse whisker sensory thalamus (V2 VPm) receives generally a single afferent fiber originating from the whisker-representing trigeminal nucleus (PrV2). Recently, however, we have discovered that transection of the whisker sensory nerve newly recruits multiple afferent fibers onto a relay neuron in the V2 VPm from the fifth or sixth postoperative day [Takeuchi Y et al (2012) J Neurosci 32:6917-30]. To reveal relationship between this synaptic remodeling of afferent fibers and somatotopic reorganization, we here employed the Krox20-Ai14 transgenic mice, in which PrV2-origin afferent fibers are specifically labeled with fluorescent protein [Takeuchi Y et al (2014) J Neurosci 34:1258-70]. Using these mice, we found that non-PrV2-origin afferent terminals significantly increased in the V2 VPm after the transection, whereas PrV2-origin afferent terminals decreased and weakened around the same time as the synaptic remodeling. Origins of non-PrV2-origin afferent fibers after the transection included the mandibular (V3) subregions of trigeminal nuclei and the dorsal column nuclei, which normally represent body parts other than whiskers. These results indicate that the transection induces considerable retraction of PrV2-origin afferent fibers and invasion of non-PrV2-origin ones in the V2 VPm, thereby induces large-scale somatotopic reorganization.