Mechanical allodynia, pain caused by innocuous mechanical stimulation, is a characteristic symptom of neuropathic pain that develops after peripheral nerve injury (PNI). In this study, we used Thy1-ChR2 mice, a transgenic mouse line that expresses channelrhodopsin-2 in touch-sensing myelinated primary afferent fibers but not in nociceptors. Light illumination to the plantar skin of Thy1-ChR2 mice with PNI produced pain-like withdrawal behavior and increased c-FOS expression in superficial spinal dorsal horn (SDH) neurons. This light-induced pain-like behavior disappeared by silencing Aβ fibers, but was not suppressed by morphine administration. Furthermore, using pathway-selective gene expression by adeno-associated viral vectors, we demonstrated that chemogenetic silencing of primary sensory cortex (S1) neurons projecting to the SDH attenuated pain-like behavior and reduced the number of c-FOS-expressing SDH neurons evoked by photostimulation of Aβ fibers. These findings indicate that spinally projecting S1 neurons contribute to Aβ fiber-derived neuropathic allodynia.