In a normal state, sympathetic efferent activity does not elicit discharges of sensory neurons, whereas it becomes associated with and excites sensory neurons in a pathophysiological state such as injury to a peripheral nerve. Although this sympathetic-sensory interaction is reportedly adrenergic, involved subtypes of adrenoreceptors are not yet clearly revealed. The purpose of this study was to determine which adrenorceptor subtypes were involved in sympathetic-sensory interaction that was developed in rats with an experimental peripheral neuropathy. Using rats that received a tight ligation of one or two of L4-L6 spinal nerves 10~15 days previously, a recording was made from afferent fibers in microfilaments teased from the dorsal root that was in continuity with the ligated spinal nerve. Electrical stimulation of sympathetic preganglionic fibers in T13 or L1 ventral root (50 Hz, 2-5 mA. 0.5 ms pulse duration, 10 sec) was made to see if the activity of recorded afferents was modulated. About half of afferents showing spontaneous discharges responded to sympathetic stimulation, and had the conduction velocities in the A-fiber range. Most of the sympathetically induced afferent responses were excitation. This sympathetically induced excitation occurred in the dorsal root ganglion (DRG), and was blocked by yohimbine (${alpha}_2$ blocker), neither by propranolol ($eta$ blocker) not by prazosine (${alpha}_1$ blocker). The results suggest that after spinal nerve ligation, sympathetic efferents interact with sensory neurons having A-fiber axons in DRG where adrenaline released from sympathetic nerve endings excites the activity of sensory neurons by acting on 2-adrenoreceptors. This 2-adrenoreceptor mediated excitation of sensory neurons may account for sympathetic involvement in neuropathic pain.