Mechanical allodynia is a symptom of neuropathic pain and is elicited by tactile stimulation. Recently, we have identified a spinal dorsal horn (SDH) inhibitory interneuron subset (operated by AAV vectors including a neuropeptide Y promoter; AAV-NpyP⁺ neurons) whose dysfunction is critical for neuropathic allodynia. Indeed, after peripheral nerve injury (PNI), these neurons exhibit deeper resting membrane potentials (RMP) and reduce excitability. However, the mechanism of these changes remains unclear. In this study, we show that the PNI-induced deepened RMP and hypoexcitability of AAV-NpyP⁺ neurons were normalized by SDH astrocyte-specific expression of a dominant negative form of STAT3 (dnSTAT3) that suppresses reactive state of astrocytes. Astrocytic dnSTAT3 expression also attenuated Aβ fiber-derived neuropathic allodynia. Conversely, induction of reactive state of SDH astrocytes by expressing a constitutive active form of STAT3 (caSTAT3) in normal rats resulted in reducing activity of AAV-NpyP⁺ neurons and causing allodynia-like behavior. Our findings indicate that reactive astrocytes in the SDH are necessary and sufficient to cause dysfunction of AAV-NpyP⁺ neurons after PNI and neuropathic allodynia. Thus, inhibiting reactive state of astrocytes could be a new therapeutic target for neuropathic allodynia.