Chronic itch is a cardinal symptom observed in patients with atopic dermatitis. Existing treatments are largely ineffective. Recent studies have identified an interneuron subpopulation expressing gastrin-releasing peptide receptors (GRPR) in the spinal dorsal horn (SDH) that is crucial for itch transmission. However, functional alterations in GRPR⁺ neurons under chronic itch conditions remain poorly understood. In this study, we used NC/Nga mice as a model of atopic dermatitis. These mice spontaneously displayed scratching behavior under conventional (CV) but not SPF conditions. For whole-cell patch-clamp recording of GRPR⁺ SDH neurons of these mice, we visualized these neurons by intraspinally microinjection of adeno-associated virus (AAV) which had a construct expressing mCherry under the control of GRPR promoter. We confirmed that mCherry⁺ cells were located in the superficial neuron in the SDH, displayed the delayed firing pattern (an index of excitatory interneurons) and were depolarized by GRP application. We recorded spontaneous and miniature EPSCs of mCherry⁺ neurons of SPF- and CV-NC/Nga mice and found an increase in the frequency, but not the amplitude, of EPSCs in mCherry⁺ neurons of CV-NC/Nga mice. These results suggest thst the activity of GRPR⁺ neurons in the SDH is facilitated under chronic itch conditions.