Mechanical allodynia is one of the symptoms of neuropathic pain and is produced by tactile stimulation. Recently, we have identified a subset of spinal dorsa horn (SDH) inhibitory interneurons that is operated by adeno-associated viral (AAV) vectors incorporating a neuropeptide Y promoter (AAV-NpyP⁺). In a model of neuropathic pain caused by peripheral nerve injury (PNI), these neurons exhibit deeper resting membrane potentials, and their excitability is impaired, which are necessary for neuropathic allodynia. However, the mechanism underlying these changes remains unknown. In this study, we show that the dysfunction of AAV-NpyP⁺ neurons require astrocytes that are activated in the SDH after PNI. We found that inhibition of PNI-induced activation of SDH astrocytes by expressing a dominant negative form of STAT3 (dnSTAT3: an inactive mutant STAT3) alleviated Aβ fiber-derived neuropathic allodynia and normalized alterations in resting membrane potentials and excitability of AAV-NpyP⁺ neurons. Our findings suggest that suppressing activation of astrocytes after PNI restores normal AAV-NpyP neurons activity and attenuates neuropathic allodynia. Thus, inhibiting astrocytes activation may be a new therapeutic target for neuropathic allodynia.