The role of mitochondria in cocaine addiction

Claire Thornton, Etty Grad, Rami Yaka

Research output: Contribution to journalReview articlepeer-review

12 Scopus citations

Abstract

The incidence of cocaine abuse is increasing especially in the U.K. where the rates are among the highest in Europe. In addition to its role as a psychostimulant, cocaine has profound effect on brain metabolism, impacting glycolysis and impairing oxidative phosphorylation. Cocaine exposure alters metabolic gene expression and protein networks in brain regions including the prefrontal cortex, the ventral tegmental area and the nucleus accumbens, the principal nuclei of the brain reward system. Here, we focus on how cocaine impacts mitochondrial function, in particular through alterations in electron transport chain function, reactive oxygen species (ROS) production and oxidative stress (OS), mitochondrial dynamics and mitophagy. Finally, we describe the impact of cocaine on brain energy metabolism in the developing brain following prenatal exposure. The plethora of mitochondrial functions altered following cocaine exposure suggest that therapies maintaining mitochondrial functional integrity may hold promise in mitigating cocaine pathology and addiction.

Original languageEnglish
Pages (from-to)749-764
Number of pages16
JournalBiochemical Journal
Volume478
Issue number4
DOIs
StatePublished - 26 Feb 2021
Externally publishedYes

Bibliographical note

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© 2021 Portland Press Ltd. All rights reserved.

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