How does the activation of DC pathways by ulnar MS suppress drug-seeking behaviors? The LHb, an epithalamic structure, projects to the VTA and the RMTg, which contain GABA neurons that inhibit DAergic activity and the behavioral effects of drugs of abuse19. Electrical stimulation of LHb neurons elicits a strong inhibition of VTA DA neurons, while inhibition of the LHb is associated with the activation of DA neurons18. Activation of the habenula reduces addiction to cocaine, nicotine, morphine and ethanol19, 30, 31, while lesions of the habenula increase drug seeking behaviors32. Our findings demonstrate that ulnar MS increased both local temperature and c-fos expression in LHb neurons projecting to the VTA/RMTg regions and LHb lesions blocked ulnar inhibition of cocaine locomotion, indicating that excitation of habenula neurons by ulnar MS can suppress psychomotor responses or NAc-neuronal activity to cocaine (Figs 4–6). Taken together, these findings provide convincing evidence that the DC somatosensory pathway is functionally linked to the LHb-VTA/RMTg pathway, which may underlie somatosensory inhibition of cocaine-induced psychomotor behaviors. Although the LHb has been shown to receive somatosensory inputs16, 20, it is not known yet how somatosensory inputs enter the LHb, which receives input from structures, such as the prefrontal cortex, lateral hypothalamus and entopeduncular nucleus33. As there are no known direct pathways projecting from VPL to the LHb, linking DC somatosensory inputs to the LHb may require multi-synaptic pathways. Lesions of the VPL abolished neuronal activation of LHb by peripheral stimulation, suggesting a putative VPL-LHb link. Others have shown that the VPL projects to prefrontal cortex34, which sends excitatory inputs to the LHb35. Connections between the VPL and LHb may be linked via the prefrontal cortex, which requires further elucidation. Regardless, previous studies have demonstrated that LHb neurons are sensitive to noxious stimuli. For example, LHb neurons respond to peripheral noxious stimuli16 and the expression of the immediately early gene c-fos in LHb is induced after noxious stimuli36. Our findings suggest that innocuous stimulation of the ulnar nerve would activate LHb neurons, as measured by local temperature, c-fos expression and in vivo extracellular recordings in the LHb. Thus, there is the possibility that noxious as well as innocuous stimuli can activate LHb neurons under certain conditions and inhibit psychomotor response to cocaine.