Subthalamic nucleus high frequency stimulation prevents and reverses escalated cocaine use

One of the key features of addiction is the escalated drug intake. The neural mechanisms involved in the transition to addiction remain to be elucidated. Since abnormal neuronal activity within the subthalamic nucleus (STN) stands as potential general neuromarker common to impulse control spectrum d...

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Bibliographic Details
Published in:Molecular psychiatry 2018-12, Vol.23 (12), p.2266-2276
Main Authors: Pelloux, Yann, Degoulet, Mickaël, Tiran-Cappello, Alix, Cohen, Candie, Lardeux, Sylvie, George, Olivier, Koob, George F., Ahmed, Serge H., Baunez, Christelle
Format: Article
Language:English
Subjects:
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Action Potentials - physiology
Addiction
Addictions
Animals
Behavioral Sciences
Biological Psychology
Care and treatment
Cocaine
Cocaine - pharmacology
Cocaine-Related Disorders - metabolism
Cocaine-Related Disorders - physiopathology
Cognitive science
Drug abuse
Drug addiction
Drug self-administration
Electrical stimuli
Health aspects
Immediate Communication
Impulsive behavior
Life Sciences
Male
Medical research
Medicine
Medicine & Public Health
Narcotics
Neurobiology
Neurons
Neurons - physiology
Neurons and Cognition
Neuroscience
Neurosciences
Obsessive compulsive disorder
Oscillations
Pharmaceutical sciences
Pharmacology
Pharmacotherapy
Psychiatry
Psychology and behavior
Rats
Recurrence (Disease)
Self Administration
Solitary tract nucleus
Stimulation
Substance abuse treatment
Subthalamic nucleus
Subthalamic Nucleus - drug effects
Theta rhythms
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Summary:One of the key features of addiction is the escalated drug intake. The neural mechanisms involved in the transition to addiction remain to be elucidated. Since abnormal neuronal activity within the subthalamic nucleus (STN) stands as potential general neuromarker common to impulse control spectrum deficits, as observed in obsessive–compulsive disorders, the present study recorded and manipulated STN neuronal activity during the initial transition to addiction (i.e., escalation) and post-abstinence relapse (i.e., re-escalation) in rats with extended drug access. We found that low-frequency (theta and beta bands) neuronal oscillations in the STN increase with escalation of cocaine intake and that either lesion or high-frequency stimulation prevents the escalation of cocaine intake. STN–HFS also reduces re-escalation after prolonged, but not short, protracted abstinence, suggesting that STN–HFS is an effective prevention for relapse when baseline rates of self-administration have been re-established. Thus, STN dysfunctions may represent an underlying mechanism for cocaine addiction and therefore a promising target for the treatment of addiction.
ISSN:1359-4184
1476-5578
DOI:10.1038/s41380-018-0080-y