Systemic injection of cocaine (15 mg/kg, i.p.) markedly increased locomotor activity, which lasted for approximately 60 min from the peak magnitude at 10 min (Con; Fig. 1A). Mechanical stimulation (MS) of the ulnar area (Ulna MS) near HT7 acupoint for 20 sec, which is sufficient to activate A- and C-fibers11, attenuated cocaine enhancement of locomotor activity, while MS of the radial site did not alter cocaine-induced locomotor activity (Rad MS; Fig. 1A). Mechanical stimulation of the ulnar site after sectioning the ulnar nerve had no effect on cocaine-induced locomotion (Fig. 1B; p > 0.05), suggesting that somatosensory-induced inhibition of cocaine-induced locomotion was mediated through activation of the ulnar nerve. Ulna MS did not affect locomotor activity in saline-injected rats (Fig. 1C), suggesting that Ulna MS attenuated cocaine-evoked locomotion, but not generalized locomotion. As ulnar MS produced consistent and reproducible inhibitory effects on cocaine-induced locomotion in our previous11 and present studies; MS was applied only to the ulnar site in subsequent experiments.Figure 1Mechanical stimulation of the ulnar nerve suppresses cocaine-induced locomotor activity. (A) Mechanical stimulation (MS) of the ulnar site (Ulna MS; n = 6) significantly attenuated the locomotor response to cocaine, compared to the control group that received cocaine only (Con; n = 6) *p < 0.05 vs. Con; # p < 0.05 vs. Rad MS. Mechanical stimulation of the radial site (Rad MS; n = 6) did not alter cocaine-induced locomotion. (B) The inhibitory effect of ulnar MS on cocaine locomotion was not observed in rats with ulnar nerve injury (Ulna X + Ulna MS; n = 8) when compared to control rats with ulnar nerve injury (Ulna X; n = 8). The term ‘X’ denotes lesion or injury. (C) Ulna MS did not affect locomotion in the control rats injected with saline (Ulna MS; n = 5).