High-Frequency Stimulation of Nucleus Accumbens Changes in Dopaminergic Reward Circuit

Yan, Ning; Chen, Ning; Zhu, Honghua; Zhang, Jianguo; Sim, Moira; Ma, Yu; Wang, Wei

doi:10.1371/journal.pone.0079318

Cited by 23 publications

(22 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Converging evidence suggests aberrant frontostriatal glutamatergic signaling in OCD (Wu et al, 2012). Moreover, electrophysiological animal work indicates that the efficacy of ventral striatal DBS for OCD may depend on restored glutamatergic OFC control over striatal regions (McCracken et al, 2007;Yan et al, 2013), which might also explain the anti-compulsive effects of glutamatergic agents such as ketamine (Rodriguez et al, 2013). It was recently hypothesized that glutamatergic frontostriatal changes may also be critical for the transition of regular to compulsive drug use (van Huijstee and Mansvelder, 2015) and glutamatergic agents are promising interventions for the treatment of substance-use and gambling disorders (Pettorruso et al, 2014).…”

Section: Glutamatementioning

confidence: 99%

Compulsivity in obsessive–compulsive disorder and addictions

Figee

Pattij

Willuhn

et al. 2016

European Neuropsychopharmacology

202

117

View full text Add to dashboard Cite

Compulsive behaviors are driven by repetitive urges and typically involve the experience of limited voluntary control over these urges, a diminished ability to delay or inhibit these behaviors, and a tendency to perform repetitive acts in a habitual or stereotyped manner. Compulsivity is not only a central characteristic of obsessive-compulsive disorder (OCD) but is also crucial to addiction. Based on this analogy, OCD has been proposed to be part of the concept of behavioral addiction along with other non-drug-related disorders that share compulsivity, such as pathological gambling, skin-picking, trichotillomania and compulsive eating. In this review, we investigate the neurobiological overlap between compulsivity in substance-use disorders, OCD and behavioral addictions as a validation for the construct of compulsivity that could be adopted in the Research Domain Criteria (RDoC). The reviewed data suggest that compulsivity in OCD and addictions is related to impaired reward and punishment processing with attenuated dopamine release in the ventral striatum, negative reinforcement in limbic systems, cognitive and behavioral inflexibility with diminished serotonergic prefrontal control, and habitual responding with imbalances between ventral and dorsal frontostriatal recruitment. Frontostriatal abnormalities of compulsivity are promising targets for neuromodulation and other interventions for OCD and addictions. We conclude that compulsivity encompasses many of the RDoC constructs in a trans-diagnostic fashion with a common brain circuit dysfunction that can help identifying appropriate prevention and treatment targets.

show abstract

Section: Glutamatementioning

confidence: 99%

Compulsivity in obsessive–compulsive disorder and addictions

Figee

Pattij

Willuhn

et al. 2016

European Neuropsychopharmacology

202

117

View full text Add to dashboard Cite

show abstract

“…Also, glutamatergic efferent projections from the amygdala to the NAcore are involved in Pavlovian responding to cue-conditioned and heroin-primed reinstatement of heroin seeking (Fuchs and See, 2002;Jones et al, 2010;Rogers et al, 2008;See et al, 2003). In line with these findings, morphine-induced CPP has been shown to increase glutamate levels in the NA, which were reduced by NAcore DBS (Yan et al, 2013). Additionally, glutamate levels in the ventral pallidum (VP) and the ventral tegmental area (VTA) were reduced, whereas GABA levels in NA, VP and VTA were increased by NAcore DBS, thereby reversing the effects of morphine CPP on glutamate and GABA release (Yan et al, 2013).…”

Section: Mechanism Of Dbsmentioning

confidence: 62%

Deep brain stimulation of the nucleus accumbens core but not shell reduces motivational components of heroin taking and seeking in rats

Schippers

Gaastra

Mesman

et al. 2017

Brain and Neuroscience Advances

View full text Add to dashboard Cite

Background: Deep brain stimulation is explored as a new intervention for treatment-resistant substance use dependence. A candidate brain region is the nucleus accumbens, due to its involvement in reward and motivation. This study aimed to explore effects of NAcore and NAshell deep brain stimulation on aspects of heroin taking and seeking in a self-administration model for rats. Methods: NAcore and NAshell deep brain stimulation was applied during 25 or 100 µg/kg/infusion heroin self-administration on an FR4 schedule of reinforcement and during cue-and heroin-induced reinstatement. In a separate group, effects of NAcore deep brain stimulation on heroin selfadministration on a progressive ratio schedule and the first extinction session were examined. Results: NAcore and NAshell deep brain stimulation did not alter heroin self-administration on an FR4 schedule. NAcore deep brain stimulation decreased cue -but not drug-induced reinstatement of heroin seeking, whereas NAshell deep brain stimulation did not affect reinstatement responding. In the second experiment, NAcore deep brain stimulation reduced responding during a progressive ratio schedule of heroin reinforcement. Finally, deep brain stimulation facilitated extinction from day 1 throughout the course of extinction learning. Conclusion: Taken together, the differential effects of NAcore and NAshell deep brain stimulation on heroin taking and seeking are in line with the distinct functional roles of these sub-regions therein. Conditioned cues have been shown to be very powerful stimuli for the persistence of addiction and relapse to drug use. Therefore, the present findings that NAcore deep brain stimulation decreases motivation for heroin taking and cue-conditioned behaviour and facilitates extinction learning are very promising, supporting the positive findings from clinical case studies.

show abstract

“…Local perfusion of morphine attenuates on the release of extracellular glutamate and increases GABA release in the NAc [21], whereas chronic morphine treatment (intraperitoneal) increases the extracellular level of glutamate and decreases the GABA release [22]. The alternation of extracellular glutamate and GABA may also occur in our work, which needs further investigation.…”

Section: Activation Of D1 Receptors Inhibits Mor-ltp By the Direct D1mentioning

confidence: 73%

Activation of the D1 receptors inhibits the long-term potentiation in vivo induced by acute morphine administration through a D1–GluN2A interaction in the nucleus accumbens

et al. 2014

View full text Add to dashboard Cite

Dopamine D1-like receptors can modulate glutamate-mediated excitatory synaptic neurotransmission, but the underlying molecular mechanism remains elusive. Here, we report that acute in-vivo morphine administration induces the long-term potentiation (Mor-LTP) of field excitatory postsynaptic potentials at the prefrontal cortex-to-nucleus accumbens shell synapses, and this process requires the activation of GluN2A-containing N-methyl-D-aspartate receptors. This Mor-LTP is completely inhibited by the D1-like receptor agonist SKF81297, but not by the D2-like receptor agonist quinpirole. SKF81297-inhibited Mor-LTP is restored by pretreatment with the TAT-conjugated interfering peptide TAT-D1-t3, which is a synthetic blocker of the direct D1-GluN2A receptor interaction. These results indicate that the activation of D1 receptors modulates Mor-LTP by the direct D1-GluN2A interaction at the prefrontal cortex-to-nucleus accumbens shell synapses and might play a role in addiction-related plastic alterations.

show abstract

High-Frequency Stimulation of Nucleus Accumbens Changes in Dopaminergic Reward Circuit

Cited by 23 publications

References 51 publications

Compulsivity in obsessive–compulsive disorder and addictions

Compulsivity in obsessive–compulsive disorder and addictions

Deep brain stimulation of the nucleus accumbens core but not shell reduces motivational components of heroin taking and seeking in rats

Activation of the D1 receptors inhibits the long-term potentiation in vivo induced by acute morphine administration through a D1–GluN2A interaction in the nucleus accumbens

Contact Info

Product

Resources

About