Converging Evidence for a Fronto-Basal-Ganglia Network for Inhibitory Control of Action and Cognition: Figure 1.

Aron, Adam R.; Durston, Sarah; Eagle, Dawn M.; Logan, Gordon D.; Stinear, Cathy M.; Stuphorn, Veit

doi:10.1523/jneurosci.3644-07.2007

Cited by 487 publications

(419 citation statements)

References 63 publications

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“…The NAcb has been widely associated with impulsive behavior in humans and rodents (Cardinal et al, 2001;Aron et al, 2007;Pattij and Vanderschuren, 2008). We have reported that spontaneously high impulsive rats on the 5-CSRT task exhibit a decrease in DA D2/3 receptor availability in the ventral striatum, including the NAcb (Dalley et al, 2007).…”

Section: Discussionmentioning

confidence: 98%

Dissociable Control of Impulsivity in Rats by Dopamine D2/3 Receptors in the Core and Shell Subregions of the Nucleus Accumbens

Besson

Belin

McNamara

et al. 2009

Neuropsychopharmacol

122

111

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Previous research has identified the nucleus accumbens (NAcb) as an important brain region underlying inter-individual variation in impulsive behavior. Such variation has been linked to decreased dopamine (DA) D2/3 receptor availability in the ventral striatum of rats exhibiting spontaneously high levels of impulsivity on a 5-choice serial reaction time (5-CSRT) test of sustained visual attention. This study investigated the involvement of DA D2/3 receptors in the NAcb core (NAcbC) and the NAcb shell (NAcbS) in impulsivity. We investigated the effects of a DA D2/3 receptor antagonist (nafadotride) and a DA D2/3 partial agonist (aripiprazole) infused directly into either the NAcbC or NAcbS of rats selected for high (HI) and low (LI) impulsivity on the 5-CSRT task. Nafadotride increased significantly the level of impulsivity when infused into the NAcbS, but decreased impulsivity when infused into the NAcbC of HI rats. By contrast, intraNAcb microinfusions of aripiprazole did not affect impulsivity. Systemic administration of nafadotride had no effect on impulsive behavior but increased the number of omissions and correct response latencies, whereas systemic injections of aripiprazole decreased impulsive and perseverative behavior, and increased the number of omissions and correct response latencies. These findings indicate an opponent modulation of impulsive behavior by DA D2/3 receptors in the NAcbS and NAcbC. Such divergent roles may have relevance for the etiology and treatment of clinical disorders of behavioral control, including attention-deficit hyperactivity disorder and drug addiction.

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Section: Discussionmentioning

confidence: 98%

Dissociable Control of Impulsivity in Rats by Dopamine D2/3 Receptors in the Core and Shell Subregions of the Nucleus Accumbens

Besson

Belin

McNamara

et al. 2009

Neuropsychopharmacol

122

111

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“…Although we cannot completely rule out the possibility that the AI/IFG activation may reflect an aversive response to other-regarding choices among selfish individuals, the correlation between AI/IFG activation and the average RTs across individuals suggests that additional cognitive processes may be engaged during the OTHER condition. It is also noteworthy that AI/IFG has been strongly implicated in cognitive control and self-regulation (46)(47)(48)(49). Given that an increase in AI/IFG activity weakened the MPFC-striatum coupling during choices for others, selfish individuals seem to use additional cognitively demanding processes that interrupt the process of prosocial valuation, which may involve signal propagation through the MPFC-striatum loops.…”

Section: Discussionmentioning

confidence: 99%

Spatial gradient in value representation along the medial prefrontal cortex reflects individual differences in prosociality

Sul

Tobler

Hein

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

127

112

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Despite the importance of valuing another person's welfare for prosocial behavior, currently we have only a limited understanding of how these values are represented in the brain and, more importantly, how they give rise to individual variability in prosociality. In the present study, participants underwent functional magnetic resonance imaging while performing a prosocial learning task in which they could choose to benefit themselves and/or another person. Choice behavior indicated that participants valued the welfare of another person, although less so than they valued their own welfare. Neural data revealed a spatial gradient in activity within the medial prefrontal cortex (MPFC), such that ventral parts predominantly represented self-regarding values and dorsal parts predominantly represented other-regarding values. Importantly, compared with selfish individuals, prosocial individuals showed a more gradual transition from selfregarding to other-regarding value signals in the MPFC and stronger MPFC-striatum coupling when they made choices for another person rather than for themselves. The present study provides evidence of neural markers reflecting individual differences in human prosociality.R anging from small acts of kindness in daily life to self-sacrificing altruism under life-threatening situations, we often observe large individual differences in how humans value another person's welfare. This differential valuation process seems to be the key to understanding various human prosocial behaviors, which are fundamental to the sustainability of human society (1). The underlying neural mechanisms and their relationship to individual differences in prosociality remain unclear, however.Perhaps the most powerful way of assessing how an outcome is valued is to use an instrumental learning paradigm that examines whether the occurrence of a response increases when it is followed by that outcome (2). The mechanisms underlying this type of learning have been described more formally with a computational model, known as the advantage learning model (3-5), which has been used successfully to reveal the neuroanatomical substrates of subjective valuation (3,4,6). Previous research has further refined the neurobiological model of reinforcement learning by emphasizing the specific roles played by the medial frontal cortex and the striatum; the medial frontal cortex computes the value of the chosen action, whereas the striatum processes reward prediction errors during reinforcement learning (4, 6-10).Unlike our current understanding of the valuation process for self-regarding choices (3, 6-12), it is much less clear whether learning also can be driven by other-regarding values, and whether this other-regarding valuation relies on the same mechanisms of reinforcement learning as those used for self. Moreover, despite the rapidly accumulating research on reward processing in social domains (13-19), the question remains of how neural representation of self-regarding vs. other-regarding values is related to individual differen...

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“…While much sparser than the indirect pathway, the hyperdirect projection has received increasing attention. By circumventing the striatum, it may provide a mechanism for cortical inputs to influence GPi and SNr output with shorter latencies and thereby assist in situations that require rapid Bstop^responses to external and internal triggers [17,19,[28][29][30][31][32][33][34][35][36][37][38][39][40][41].…”

Section: Functional/anatomic Considerations Of the Basal Ganglia Circmentioning

confidence: 99%

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

2016

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Deep brain stimulation (DBS) is highly effective for both hypo-and hyperkinetic movement disorders of basal ganglia origin. The clinical use of DBS is, in part, empiric, based on the experience with prior surgical ablative therapies for these disorders, and, in part, driven by scientific discoveries made decades ago. In this review, we consider anatomical and functional concepts of the basal ganglia relevant to our understanding of DBS mechanisms, as well as our current understanding of the pathophysiology of two of the most commonly DBS-treated conditions, Parkinson's disease and dystonia. Finally, we discuss the proposed mechanism(s) of action of DBS in restoring function in patients with movement disorders. The signs and symptoms of the various disorders appear to result from signature disordered activity in the basal ganglia output, which disrupts the activity in thalamocortical and brainstem networks. The available evidence suggests that the effects of DBS are strongly dependent on targeting sensorimotor portions of specific nodes of the basal gangliathalamocortical motor circuit, that is, the subthalamic nucleus and the internal segment of the globus pallidus. There is little evidence to suggest that DBS in patients with movement disorders restores normal basal ganglia functions (e.g., their role in movement or reinforcement learning). Instead, it appears that high-frequency DBS replaces the abnormal basal ganglia output with a more tolerable pattern, which helps to restore the functionality of downstream networks.

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Converging Evidence for a Fronto-Basal-Ganglia Network for Inhibitory Control of Action and Cognition: Figure 1.

Cited by 487 publications

References 63 publications

Dissociable Control of Impulsivity in Rats by Dopamine D2/3 Receptors in the Core and Shell Subregions of the Nucleus Accumbens

Dissociable Control of Impulsivity in Rats by Dopamine D2/3 Receptors in the Core and Shell Subregions of the Nucleus Accumbens

Spatial gradient in value representation along the medial prefrontal cortex reflects individual differences in prosociality

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

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