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Related Concept Videos

CNS Stimulants: Cocaine, Amphetamines and Cannabinoids01:24

CNS Stimulants: Cocaine, Amphetamines and Cannabinoids

199
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...
199

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Using Optogenetics to Reverse Neuroplasticity and Inhibit Cocaine Seeking in Rats
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Exercise Modifies the Brain Metabolic Response to Chronic Cocaine Exposure Inhibiting the Stria Terminalis.

Colin Hanna1, Rutao Yao2, Munawwar Sajjad2

  • 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.

Brain Sciences
|December 23, 2023
PubMed
Summary

Aerobic exercise alters brain glucose metabolism in cocaine-exposed rats, affecting regions involved in reward and stress. This research highlights exercise

Keywords:
18F-FDG fluorodeoxyglucoseaerobic exercisecocaineglucose metabolismpositron emission tomographyratstatistical parametric mapping

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Area of Science:

  • Neuroscience
  • Exercise Physiology
  • Addiction Research

Background:

  • Exercise is known to benefit mental and physiological health.
  • Physical activity plays a protective role in various diseases, including neurological and psychiatric conditions.
  • Understanding exercise's impact on the brain's response to drugs of abuse is crucial.

Purpose of the Study:

  • To investigate the effects of aerobic exercise on brain glucose metabolism in female rats with chronic cocaine exposure.
  • To identify specific brain regions where metabolic activity is altered by exercise in the context of cocaine use.

Main Methods:

  • Utilizing positron emission tomography (PET) with [18F]-Fluorodeoxyglucose (FDG) to measure brain glucose metabolism.
  • Comparing brain metabolic activity between an exercise group (treadmill running for six weeks) and a sedentary control group, both exposed to chronic cocaine.
  • Analyzing metabolic changes in distinct brain regions.

Main Results:

  • Aerobic exercise led to significant metabolic changes in response to chronic cocaine exposure.
  • Observed activation in the secondary visual cortex.
  • Observed inhibition in the cerebellum, stria terminalis, thalamus, caudate putamen, and primary somatosensory cortex.

Conclusions:

  • Chronic aerobic exercise can modify the brain's metabolic response to cocaine treatment.
  • These alterations occur in brain circuits associated with emotion, behavior, and the reward system.
  • Findings support exercise as a potential modulator of the brain's response to drugs of abuse, offering avenues for future research in addiction and neuroscience.