Date of Graduation


Document Type


Degree Type



Eberly College of Arts and Sciences



Committee Chair

Karen G. Anderson

Committee Co-Chair

Regina A. Carroll

Committee Member

Regina A. Carroll

Committee Member

Steven G. Kinsey


Delay discounting is a measure of impulsive choice that is correlated with maladaptive behavior and psychological disorders. Disruptions to serotonin and dopamine pathways can cause changes in delay discounting, as can lesions to the prefrontal cortex and nucleus accumbens. The endocannabinoid system modulates other neurotransmitter systems, including dopamine and serotonin pathways. Cannabinoid receptors type 1 are found in relatively high concentrations in the nucleus accumbens and the prefrontal cortex. These receptors are activated by endogenous cannabinoids, which are synthesized on demand and broken down by catabolic enzymes. The action of these enzymes can be inhibited by a class of drugs known as cannabinoid enzyme inhibitors, which ultimately produce higher levels of endogenous cannabinoids by preventing their catabolic degradation. The present study examined effects of two cannabinoid enzyme inhibitors, URB597 and JZL195, on delay discounting in rats. Delay discounting was measured at baseline and after drug administration. Area under the curve and indifference points were not affected by any dose of either drug, but 7.5 mg/kg of JZL195 decreased percent larger-reinforcer choice at the lowest delay value and increased it at the highest delay value. URB597 increase percent larger-reinforcer choice only at one intermediate delay value. JZL195 increased response latencies at the 7.5 mg/kg dose. No systematic, dose-dependent effect of either drug on measures of delay discounting was observed.