Exercise Modulates Brain Glucose Utilization Response to Acute Cocaine

Exercise, a proven method of boosting health and wellness, is thought to act as a protective factor against many neurological and psychological diseases. Recent studies on exercise and drug exposure have pinpointed some of the neurological mechanisms that may characterize this protective factor. Using positron emission tomography (PET) imaging techniques and the glucose analog [(18)F]-Fluorodeoxyglucose ((18)F-FDG), our team sought to identify how chronic aerobic exercise modulates brain glucose metabolism (BGluM) after drug-naïve rats were exposed to an acute dose of cocaine. Using sedentary rats as a control group, we observed significant differences in regional BGluM. Chronic treadmill exercise treatment coupled with acute cocaine exposure induced responses in BGluM activity in the following brain regions: postsubiculum (Post), parasubiculum (PaS), granular and dysgranular insular cortex (GI and DI, respectively), substantia nigra reticular (SNR) and compact part dorsal tier (SNCD), temporal association cortex (TeA), entopenduncular nucleus (EP), and crus 1 of the ansiform lobule (crus 1). Inhibition, characterized by decreased responses due to our exercise, was found in the ventral endopiriform nucleus (VEn). These areas are associated with memory and various motor functions. They also include and share connections with densely dopaminergic areas of the mesolimbic system. In conclusion, these findings suggest that treadmill exercise in rats mediates brain glucose response to an acute dose of cocaine differently as compared to sedentary rats. The modulated brain glucose utilization occurs in brain regions responsible for memory and association, spatial navigation, and motor control as well as corticomesolimbic regions related to reward, emotion, and movement.