Dr. Schank’s Lab
Director: Jesse R. Schank, PhD
The neurokinin-1 receptor (NK1R) serves as the primary target of the neuroactive peptide substance P and mediates stress, anxiety, and reward. Similar to inhibition of other stress-related neuropeptides, NK1R antagonism attenuates stress-induced reinstatement of alcohol seeking, but leaves primary reinforcement and cue-induced reinstatement unaffected. Neuroanatomical analysis of regions that could potentially mediate this effect has identified the nucleus accumbens shell and dorsal raphe nucleus as two primary regions of interest. We have also found that NK1R antagonists selectively suppress escalated alcohol self-administration in alcohol preferring P rats. NK1Rs are upregulated in the central nucleus of the amygdala in P rats, and direct infusion of an NK1R antagonist reverses escalated self-administration in these animals. Consistent with our findings with stress-induced reinstatement of alcohol seeking, we found that NK1R antagonism attenuates stress-induced reinstatement of cocaine seeking, but does not affect baseline cocaine self-administration. This suggests that NK1R antagonism mediates stress-induced seeking of multiple drug classes. Future experiments will explore the effects of NK1R upregulation on alcohol self-administration and reinstatement, the effect of chronic stressors on NK1R expression and alcohol seeking, and the downstream intracellular signaling mechanisms that mediate these processes.
R00 AA021805 - "The role of the neurokinin-1 receptor and NF kappa B in alcohol-induced behavior" - 12/2012-present