Our previous and present studies demonstrated that innocuous, mechanical stimulation of the ulnar nerve at HT7, an acupoint at the ulnar nerve, suppresses drug-seeking behaviors and drug-induced DA release in NAc11, 12, 25, 27. During such stimulation, the superficial or deep afferents of ulnar nerve are activated and the afferent signals are transmitted via A-fiber of ulnar nerve11. The afferent inputs reduce drug-induced DA release in the NAc by normalizing the decreased activity of VTA GABA neurons in addicted rats9, 12, 22. While our previous and present studies demonstrated that under drug-induced conditions, innocuous sensory inputs produced a consistent suppression of psychomotor behaviors and DA release11, 12, 25, 27, others have shown mixed results in responses of midbrain DA neurons to innocuous stimulation in drug-naïve conditions. For examples, non-noxious stimuli such as foot pressure and cervical probing elicit short latency facilitation or inhibition of midbrain DA neurons in drug-naïve rats28. Innocuous sensory stimulation by electrical stimulation or 80–100 mmHg pressure to the skin can produce a slight decrease in DA release in the dorsal striatum4, 5 or a mild increase in DA release in the NAc15. This discrepancy may be due to anatomical segregation of functional subgroups in midbrain DA neurons responding to sensory stimuli. In support of this, one previous study demonstrated that DA neurons activated by sensory stimuli are located dorsolaterally in the substantia nigra pars, while DA neurons inhibited by the stimuli are found ventromedially, some in the VTA29. In the present study, the afferent inputs, which were conveyed via DC pathway, attenuated cocaine-induced c-fos expression in NAc. It led to the speculation that afferent inputs from cutaneous innocuous stimuli would inhibit DA neurons in the VTA causing a reduced DA release in NAc, thereby suppressing cocaine-induced psychomotor behaviors.