Mechanical allodynia is a debilitating symptom associated with millions of chronic pain patients.It exists in two forms,dynamic and static,which are evoked by gentle skin touch and pressure,respectively,but the underlying specific circuits remain unknown.Here we report that spinal neurons marked by the knock-in Vglut3-Cre are required to transmit dynamic,but not static,allodynia,and these neurons form morphine-resistant polysynaptic pathways to relay inputs from low-threshold Aβ mechanoreceptors to pain output neurons.