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Objective Tactile allodynia is one of the common features of peripheral neuropathy in which myelinated Aβ fibers were proven to have contributed to the behavior in animal models and patients in previous studies.Various firing patterns have been observed in Aβ fibers, though the specific firing pattern which might mediate tactile allodynia remains poorly understood.A kind of evoked-bursting (EB) was identified on Aβ neurons on a neuropathic pain model, the present study is to explore the characteristics of EB, whether there are causal link between EB and allodynia, and also the ion mechanism underlying the EB.Methods Chronic compression of dorsal root ganglion (DRG) models (CCD model) were prepared for tactile allodynia test.In vivo intracellular recording, extracellular recording and in vitro patch-clamp recording were used for the observation of activity of DRG neurons and wide dynamic range (WDR) neurons.Results In CCD models, dominant tactile allodynia could be observed.The DRG soma became hyperexcitable with various firing patterns, in which, EB (a periphery input spike followed by the somatic burst firing) was identified on Aβ neurons with a significantly increased percentage of 43.3% compared to normal neurons (13.3%).Similar with spontaneous-bursting, a frequently observed firing pattern, the duration of EB increased with the membrane potential depolarization, and the existence of EB relied on the membrane potential oscillation.A distinct feature of EB is its dependence on periphery input especially from Aβ afferent, which should be a prerequisite for the production of tactile allodynia.After-discharge of spinal cord WDR neurons in response to peripheral Aβ strength stimulation was a distinguishing feature of spinal neural correlate of tactile allodynia.This response was suppressed after abolishing EB at DRG level, thus, we propose that EB from injured DRG neurons might act as a tactile allodynia pain signal.We further investigated the ion current mechanism underlying EB.Multiple conductances were considered in the participation of EB.INap, IDTX, and Ih were observed to work together in EB production.Conclusion EB from injured DRG Aβ neurons might act as a tactile allodynia pain signal.Therefore, the disturbance of EB on ion channel targets in combined manner would be a promising therapeutic strategy for treatment of allodynia.