Change is coming!
After a several month hiatus, I’m happy to be posting again!
This means good-bye NYC and hello Washington DC! It also means that the scope, style, and range of topics I’ll write about will greatly expand beyond just drug addiction. I’m still figuring out those details….
But in the mean time:
Cocaine Addiction Review Article
About two years ago I wrote a review article for a new academic book about addiction. Finally, the book and the article have been published!
The book is Neuropathology of Drug Addictions and Substance Misuse. My article appears in Volume 2.
Feel free to download a pdf of my article for free!
I first present an overview of the pathology and neurobiology of cocaine addiction and then discuss some of the research findings about changes that occur in the brain because of cocaine addiction.
A summary of key points discussed in the article:
- Cocaine is a widely abused drug that has significant economic, medical, and social costs and no effective pharmacotherapeutic treatments.
- Cocaine addiction progresses from initial use to repetitive cycles of heavy, short-term use (“binge” use), abstinence, and relapse.
- Unlike other drugs of abuse (which only primarily affect DA release), cocaine’s mechanism of action consists of blocking the reuptake of all monoamine neurotransmitters (DA, 5HT, and NE) by antagonizing the monoamine transporters (DAT, SERT, and NET) thus leading to an accumulation of these neurotransmitters in the synapse of the mesolimbic reward pathway and other regions of the brain.
- Genetic and environmental factors contribute to the susceptibility of an individual to becoming addicted to cocaine, and based on twin studies, it has been estimated that genetics may account for 30–60%, and as high as 78% of this susceptibility.
- Acute cocaine use activates the HPA axis while chronic cocaine use sensitizes the HPA axis and blunts the stress response, which contributes to relapse behavior.
- Accurate behavioral models used to study cocaine addiction, such as self-administration and the “binge” model, are useful because they attempt to recapitulate the human disease.
- Cocaine use results in upregulation of dynorphin mRNA and protein and subsequent elevation of KOPR/dynorphin tone in the VTA/CPu/NAc circuit in virtually every behavioral model tested.
- Modulation of the KOPR/dynorphin system may represent a viable pharmacotherapeutic target for treatment of cocaine addiction.