Deep Brain Stimulation: A potential treatment for cocaine relapse

or, technically, 
Deep brain stimulation of the nucleus accumbens shell attenuates cue-induced reinstatement of both cocaine and sucrose seeking in rats [See the original abstract on PubMed]

Authors: Leonardo A. Guercio, Heath D. Schmidt, R. Christopher Pierce

Brief prepared by: Leonardo Guercio
Brief approved by: Ari Kahn
Section Chief: David Reiner
Date posted: April 11, 2017 

Brief in Brief (TL;DR)

What do we know: Drug relapse in humans and animal models can be produced by three major factors: stress, drug-associated cues (environments and items), and re-exposure to the drug itself. The nucleus accumbens is a brain region that is critically involved in drug addiction and relapse. Deep brain stimulation (DBS), a Food and Drug Administration (FDA)-approved treatment for Parkinson's disease, of the nucleus accumbens can block cocaine relapse that is triggered by re-exposure to cocaine in animal models of addiction. 

What don’t we know: Can DBS of the nucleus accumbens also block cocaine relapse triggered by cocaine-associated cues, such as environments associated with drug use? 

What this study shows: We can effectively use DBS in the nucleus accumbens to block cocaine relapse triggered by cocaine-associated cues. However, DBS in this brain region may also affect the ability to seek naturally rewarding substances, such as sugar. 

What we can do in the future because of this study:We can figure out if DBS can become an FDA-approved treatment for drug addiction. Future findings may also help determine what other brain areas are involved in the different types of relapse, and whether DBS can be an effective treatment in all types of drug relapse. 

Why you should care: There are very few treatment options for drug addiction in general and there are no FDA-approved treatments for cocaine addiction. Existing FDA-approved treatments like DBS may be effective in treating relapse to cocaine and other drugs.

Brief for Non-Neuroscientists

A major problem facing cocaine addicts is the discouragingly high rate of relapse. Cocaine relapse in humans can be precipitated by three major factors: stress, drug-associated cues and contexts, and re-exposure to the drug itself. We can model cocaine relapse using these same factors in an animal behavior model called reinstatement. Briefly, animals are placed in an operant chamber where they can press a lever to self-administer cocaine. This is done daily for about 3 weeks, then the drug is removed and animals undergo a period of withdrawal. After approximately 1 week of withdrawal, the animals are placed back in the operant chamber, and cocaine seeking is reinstated either by an injection of cocaine, exposure to lights and tones previously paired with cocaine infusions, or a stressor. 

This reinstatement model is extremely useful for determining brain regions and neurotransmitters involved in cocaine relapse, with the hopes of developing a treatment for cocaine addiction and relapse. Currently, there are no FDA-approved therapies for cocaine addiction and relapse. Deep brain stimulation (DBS) is an FDA-approved treatment for Parkinson's disease. By applying DBS to the nucleus accumbens, a brain region critically involved in drug addiction and relapse, we were able to block cocaine reinstatement triggered by cocaine-associated cues. However, DBS in this brain region also blocked responding for sugar as well, so it may affect natural reward processing. Understanding how DBS can affect the brain regions and circuits involved in cocaine relapse may lead to repackaging DBS as a treatment for drug addiction.

Brief for Neuroscientists

Our lab has previously shown that deep brain stimulation (DBS) of the nucleus accumbens shell attenuates the priming-induced reinstatement of cocaine seeking, without perturbing sucrose reinstatement. In this study, we examined whether deep brain stimulation (DBS) can modulate cue-induced reinstatement of cocaine and sucrose seeking. We found that DBS of the accumbens shell attenuated cue-induced reinstatement of cocaine seeking. However, DBS in this region also attenuated cue-induced sucrose reinstatement, suggesting that the effects of DBS may not be drug-specific when suppressing cue-induced relapse. Further studies will examine the efficacy of DBS as a potential therapeutic avenue for cocaine reinstatement.