The role of mitochondria in cocaine addiction

Author:

Thornton Claire1ORCID,Grad Etty2,Yaka Rami2

Affiliation:

1. Department of Comparative Biomedical Sciences, Royal Veterinary College, London, U.K.

2. Institute for Drug Research (IDR), School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem 91120, Israel

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.

Publisher

Portland Press Ltd.

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference133 articles.

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2. EMCDDA (2019) European Drug Report - Trends and Developments. In European Drug Report 2019, European Monitoring Centre for Drugs and Drug Addiction, Luxenbourg

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