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The goal of this project is to evaluate the hypothesis that traumatic brain injury induces alterations in the brain s reward circuitry which may make an injured brain more susceptible to the rewarding effects of opioids. We are currently conducting experiments to evaluate the hypothesis that TBI causes changes in the analgesic response to opioids following acute and repeated drug administration. We are also testing the hypothesis that moderate TBI increases the susceptibility for opioid abuse as measured by an alteration in the rewarding properties of oxycodone. We have completed the third year of experimentation and thus far have found that TBI induces changes in oxycodone abuse-related behaviors and may induce alteration in the brain reward, particularly expression of the dopamine receptor subtype 2. All studies are on-going., The original document contains color images.

The goal of this project is to evaluate the hypothesis that traumatic brain injury induces alterations in the brain s reward circuitry which may make an injured brain more susceptible to the rewarding effects of opioids. We are currently conducting experiments to evaluate the hypothesis that TBI causes changes in the analgesic response to opioids following acute and repeated drug administration. We are secondly in the midst of testing the hypothesis that moderate TBI increases the susceptibility for opioid abuse as measured by an alteration in the rewarding properties of oxycodone. We have completed the first year of experimentation and thus far have found that the mean duration of transient unconsciousness in the animals that received TBI is consistent with a moderate injury. A trend toward increase tail withdrawal latencies was observed in the TBI group, but the number of animals per group is yet not sufficient for complete analysis. We have also observed a trend for differences between potency of oxycodone administration between TBI and sham rats. Trends for between groups differences were also seen in self-administration experiments. All studies are on-going., The original document contains color images.

The goal of this project is to evaluate the effect of a moderate-level brain injury on risk for opioid abuse using preclinical models of abuse-related behaviors in rats. Thus far we have assessed the effect of brain injury on the rewarding effects of oxycodone in two rat self-administration procedures. We have found that there are significant differences in the acquisition and maintenance of oxycodone intravenous self-administration behavior between brain-injured and control rats. Data collected to date suggest brain injured rats have a greater sensitivity to the rewarding effects of oxycodone and a greater tolerance for the use-limiting effects of oxycodone (eg. sedation, motor impairment, dysphoria). Conversely, it appears that there is no difference between brain-injured and sham controls in a model of relapse to oxycodone self-administration. Preliminary testing of oxycodone for analgesic strength and development of tolerance also has shown no difference between sham controls and brain injured subjects. Additional self-administration studies to determine the rewarding strength of oxycodone as well as development of physical dependence are ongoing., The original document contains color images.

The goal of this project is to evaluate the hypothesis that traumatic brain injury induces alterations in the brain s reward circuitry which may make an injured brain more susceptible to the rewarding effects of opioids. We are currently conducting experiments to evaluate the hypothesis that TBI causes changes in the analgesic response to opioids following acute and repeated drug administration. We are secondly in the midst of testing the hypothesis that moderate TBI increases the susceptibility for opioid abuse as measured by an alteration in the rewarding properties of oxycodone. We have completed the first year of experimentation and thus far have found that the mean duration of transient unconsciousness in the animals that received TBI is consistent with a moderate injury. A trend toward increased tail withdrawal latencies was observed in the TBI group, but the number of animals per group is yet not sufficient for complete analysis. We have also observed a trend for differences between potency of oxycodone administration between TBI and sham rats. Trends for between group differences were also seen in self-administration experiments. All studies are on-going., The original document contains color images.

The goal of this project is to evaluate the hypothesis that traumatic brain injury induces alterations in the brain's reward circuitry which may make an injured brain more susceptible to the rewarding effects of opioids. We are currently conducting experiments to evaluate the hypothesis that TBI causes changes in the analgesic response to opioids following acute and repeated drug administration. We are secondly in the midst of testing the hypothesis that moderate TBI increases the susceptibility for opioid abuse as measured by an alteration in the rewarding properties of oxycodone. We have completed the first year of experimentation and thus far have found that the mean duration of transient unconsciousness in the animals that received TBI is consistent with a moderate injury. A trend toward increase tail withdrawal latencies was observed in the TBI group, but the number of animals per group is yet not sufficient for complete analysis. We have also observed a trend for differences between potency of oxycodone administration between TBI and sham rats. Trends for between groups differences were also seen in self-administration experiments. All studies are on-going.