Subthalamic nucleus high-frequency stimulation modulates neuronal reactivity to cocaine within the reward circuit

Hachem-Delaunay, Sabira; Fournier, Marie‐Line; Cohen, Candie; Bonneau, Nicolas; Cador, Martine; Baunez, Christelle; Moine, Catherine Le

doi:10.1016/j.nbd.2015.05.007

Cited by 19 publications

(17 citation statements)

References 52 publications

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“…The present results are consistent with previous studies that reported decreases in metabolic activity (Benazzouz et al, 1995;Tai et al, 2003) and decreases in immediate-early gene levels (Creed et al, 2012) in the STN's output regions after STN HFS. Our results do not confirm previous reports that showed either no change or increases in Fos-positive neurons in the SNr and EP after STN HFS (Hachem-Delaunay et al, 2015;Shehab et al, 2014;Tan et al, 2011). Different techniques (ie, IHC vs in situ hybridization) and different times of stimulation vs sacrifice may explain these discrepancies.…”

Section: Discussioncontrasting

confidence: 99%

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High-Frequency Stimulation of the Subthalamic Nucleus Blocks Compulsive-Like Re-Escalation of Heroin Taking in Rats

Wade

Kallupi

Hernandez

et al. 2016

Neuropsychopharmacol

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Opioid addiction, including addiction to heroin, has markedly increased in the past decade. The cost and pervasiveness of heroin addiction, including resistance to recovery from addiction, provide a compelling basis for developing novel therapeutic strategies. Deep brain stimulation may represent a viable alternative strategy for the treatment of intractable heroin addiction, particularly in individuals who are resistant to traditional therapies. Here we provide preclinical evidence of the therapeutic potential of high-frequency stimulation of the subthalamic nucleus (STN HFS) for heroin addiction. STN HFS prevented the re-escalation of heroin intake after abstinence in rats with extended access to heroin, an animal model of compulsive heroin taking. STN HFS inhibited key brain regions, including the substantia nigra, entopeduncular nucleus, and nucleus accumbens shell measured using brain mapping analyses of immediate-early gene expression and produced a robust silencing of STN neurons as measured using whole-cell recording ex vivo. These results warrant further investigation to examine the therapeutic effects that STN HFS may have on relapse in humans with heroin addiction.

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Section: Discussioncontrasting

confidence: 99%

“…Microdialysis studies have shown increased levels of dopamine in the striatum after STN HFS (Winter et al, 2008). In contrast, STN HFS reduced cocaine-induced Fos expression in the NAc (Hachem-Delaunay et al, 2015). No changes were observed in the NAc core, insula, anteroventral thalamus, or VTA.…”

Section: Discussionmentioning

confidence: 97%

High-Frequency Stimulation of the Subthalamic Nucleus Blocks Compulsive-Like Re-Escalation of Heroin Taking in Rats

Wade

Kallupi

Hernandez

et al. 2016

Neuropsychopharmacol

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“…The STN has been reported to send a multitude of efferents to the basal ganglia and their associated structures, including the GPi/EP, GPe/GP, SNr, VP, pedunculopontine nucleus, SNc, and basolateral amygdala ( Kita and Kitai, 1987 ; Parent and Hazrati, 1995 ; Parent et al, 2000 ; Sato et al, 2000 ; Benarroch, 2008 ; Degos et al, 2008 ; Watabe-Uchida et al, 2012 ; Hachem-Delaunay et al, 2015 ). However, to our knowledge, no direct innervation from the STN to either the NAc or DStr has so far been identified.…”

Section: Resultsmentioning

confidence: 99%

ReducedVglut2/Slc17a6Gene Expression Levels throughout the Mouse Subthalamic Nucleus Cause Cell Loss and Structural Disorganization Followed by Increased Motor Activity and Decreased Sugar Consumption

Schweizer

Viereckel

Smith-Anttila

et al. 2016

eNeuro

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“…A recent study showed that STN stimulation in rats diminished c-Fos gene activation in the striatum that is typically observed during acute cocaine administration, suggesting that STN DBS might decrease the reinforcing properties of the drug (Hachem-Delaunay et al ., 2015). In another study, it was shown that STN-lesioned rats showed less impulsive behavior compared to non-lesioned controls in a delay-discounting task where impulsivity was defined as selection of a small immediate reward over a large delayed reward.…”

Section: A Subthalamic Locus For Valence Processingmentioning

confidence: 99%

The Subthalamic Nucleus, Limbic Function, and Impulse Control

2015

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It has been well documented that deep brain stimulation (DBS) of the subthalamic nucleus (STN) to address some of the disabling motor symptoms of Parkinson’s disease (PD) can evoke unintended effects, especially on non-motor behavior. This observation has catalyzed more than a decade of research concentrated on establishing trends and identifying potential mechanisms for these non-motor effects. While many issues remain unresolved, the collective result of many research studies and clinical observations has been a general recognition of the role of the STN in mediating limbic function. In particular, the STN has been implicated in impulse control and the related construct of valence processing. A better understanding of STN involvement in these phenomena could have important implications for treating impulse control disorders (ICDs). ICDs affect up to 40% of PD patients on dopamine agonist therapy and approximately 15% of PD patients overall. ICDs have been reported to be associated with STN DBS. In this paper we will focus on impulse control and review pre-clinical, clinical, behavioral, imaging, and electrophysiological studies pertaining to the limbic function of the STN.

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Subthalamic nucleus high-frequency stimulation modulates neuronal reactivity to cocaine within the reward circuit

Cited by 19 publications

References 52 publications

High-Frequency Stimulation of the Subthalamic Nucleus Blocks Compulsive-Like Re-Escalation of Heroin Taking in Rats

High-Frequency Stimulation of the Subthalamic Nucleus Blocks Compulsive-Like Re-Escalation of Heroin Taking in Rats

ReducedVglut2/Slc17a6Gene Expression Levels throughout the Mouse Subthalamic Nucleus Cause Cell Loss and Structural Disorganization Followed by Increased Motor Activity and Decreased Sugar Consumption

The Subthalamic Nucleus, Limbic Function, and Impulse Control

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