Graduation Year

Spring 2012

Document Type

Open Access Senior Thesis

Degree Name

Bachelor of Arts



Reader 1

Thomas Borowski

Reader 2

Melissa J. Coleman

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Terms of Use for work posted in Scholarship@Claremont.

Rights Information

© 2012 Sara K. Cronin


Previous research has shown that cannabidiol (CBD), a non-psychoactive compound in the hemp plant Cannabis sativa, may be useful in treating drug craving, one of the hallmarks of drug addiction. However, the neural mechanism by which CBD attenuates craving is poorly understood. Studies from other laboratories have shown that neuroplastic changes associated with brain NMDA glutamate systems may at least partially serve as a neural mechanism for craving. In the current study, the noncompetitive NMDA receptor antagonist MK-801 maleate was used to induce locomotor sensitization, a form of NMDA glutamate-mediated neuroplasticity, in mice to test the sensitization-attenuating potential of CBD. Separate groups of mice (N=8) received either CBD (1.0 mg/kg, i.p.) or saline thirty minutes prior to an intraperitoneal injection of MK-801 (0.5 mg/kg, i.p.) or saline and tested for locomotor performance in an open field (Induction Trial). Seventy-two hours later all mice, regardless of drug pretreatment, were tested for locomotor activity following a second administration (0.5 mg/kg, i.p.) of MK-801 (Sensitization Trial). Results revealed a significant difference across groups for the Induction Trial, with groups receiving SAL-MK801 and CBD-MK801 significantly more active than SAL-SAL and CBD-SAL groups. Pretreatment with CBD had no effect on the locomotor activating effects of MK-801 during the Sensitization Trial with similar levels of locomotor performance across drug groups. Possibilities for the lack of CBD effects are discussed, as well as implications and future research directions.