The allodynia that develops after sciatic nerve injury has been shown to involve plasticity in spinal dorsal horn inhibitory neurons that normally prevent (gate) low-threshold, primary afferent Aβ activity from reaching the nociceptive spinoparabrachial projection neurons, thereby allowing gentle touch to the hindpaw to promote paw withdrawal as if it was painful.54–60 We hypothesized that chemogenetic activation of Calca neurons may activate descending circuits to the spinal cord, resulting in plasticity that resembles that induced by nerve injury. Here, CALCA is linked to injury.