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Related Concept Videos

CNS Stimulants: Cocaine, Amphetamines and Cannabinoids01:24

CNS Stimulants: Cocaine, Amphetamines and Cannabinoids

310
CNS stimulants, such as cocaine, amphetamines, and cannabinoids, have varying structures and mechanisms of action that lead to different therapeutic effects and side effects. Cocaine, with its molecular formula C17H21NO4, is a tropane alkaloid and a tertiary amino compound. It has two chemical forms: the hydrochloride salt and the "freebase." The former is in powder form, while the latter involves removing the hydrochloride salt to create a form that can be smoked. Cocaine exerts its...
310

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Updated: Aug 16, 2025

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Exercise Modulates Brain Glucose Utilization Response to Acute Cocaine.

Colin Hanna1, John Hamilton1, Kenneth Blum2

  • 1Behavioral Neuropharmacology and Neuroimaging Laboratory on Addictions, Clinical Research Institute on Addictions, Department of Pharmacology and Toxicology, Jacob School of Medicine and Biosciences, State University of New York at Buffalo, Buffalo, NY 14203, USA.

Journal of Personalized Medicine
|December 23, 2022
PubMed
Summary

Chronic aerobic exercise alters brain glucose metabolism in rats following cocaine exposure. Exercise modulates responses in brain regions linked to memory, motor function, and reward pathways, suggesting a neuroprotective effect.

Keywords:
18F-FDG fluorodeoxyglucoseStatistical Parametric Mappingaerobic exercisecocaineglucose metabolismpositron emission tomographyrat

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Area of Science:

  • Neuroscience
  • Exercise Physiology
  • Pharmacology

Background:

  • Exercise is recognized for its health benefits and potential neuroprotective effects against neurological and psychological diseases.
  • Understanding the neurological mechanisms underlying exercise's protective role, particularly in response to drug exposure, is crucial.

Purpose of the Study:

  • To investigate how chronic aerobic exercise influences brain glucose metabolism (BGluM) in rats after acute cocaine exposure.
  • To identify specific brain regions where BGluM is modulated by exercise in the context of cocaine administration.

Main Methods:

  • Utilized positron emission tomography (PET) imaging with the glucose analog [18F]-Fluorodeoxyglucose (18F-FDG).
  • Compared BGluM in rats subjected to chronic treadmill exercise versus sedentary controls after acute cocaine exposure.

Main Results:

  • Significant differences in regional BGluM were observed between exercise and sedentary groups post-cocaine.
  • Exercise induced altered BGluM in areas including the postsubiculum, insular cortex, substantia nigra, and temporal association cortex.
  • Inhibition of BGluM was noted in the ventral endopiriform nucleus in the exercised group.

Conclusions:

  • Chronic treadmill exercise significantly alters the brain's glucose metabolic response to acute cocaine exposure in rats.
  • The observed modulations in brain regions associated with memory, motor control, and reward pathways suggest exercise-induced neuroprotection.
  • These findings highlight exercise's role in mediating neural responses to psychostimulants.