ANGER EXPRESSION, EDNOGENOUS OPHOIDS, AND ACUTE PAIN

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The Specific Aim of the study is to determine whether anger arousal is a key factor in the emergence of the link between opioid dysfunction and anger-out vis-a-vis pain sensitivity. Healthy normals will be assigned to placebo or opioid blockade (50 mg naltrexone) conditions and will perform either a cognitive task with harassment followed by pain-induction, or will undergo pain induction and then the cognitive task. If anger arousal is a key determinant in eliciting opioid-mediated differences in pain sensitivity associated with anger-out, then we expect anger-out x drug x task order interactions such that: a) under placebo, high anger-out will be related to greater pain sensitivity most strongly among subjects undergoing harassment (i.e. anger induction) prior to pain-induction; b) pharmacological blockade of the endogenous opioids underlying diminished pain responsiveness in low anger-out individuals will result in the relationships between anger-out and pain sensitivity becoming nonsignificant for both task orders. In summary, under conditions of acute anger arousal, pharmacological opioid blockade is expected to make low anger-out individuals react to pain stimulation in a manner similar to high anger-out individuals, who are expected to display opioid dysfunction.