Emotional and motivational changes after bilateral lesions of the globus pallidus.

Vijayaraghavan, Lavanya; Vaidya, Jatin G.; Humphreys, Clare T.; Beglinger, Leigh J.; Paradiso, Sergio

doi:10.1037/0894-4105.22.3.412

Cited by 38 publications

(27 citation statements)

References 26 publications

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“…We suggest that these VP neuronal signals for reward components could be related to reports of activity in human posterior VP positively correlated with pleasant food images (17) and mechanisms by which opioid and related stimulation in a VP hotspot can modulate the hedonic impact of sensory rewards (33,36,77). Conversely, one could speculate that impairment of hedonic signals in NAc-VP pathways could contribute to clinical manifestations of anhedonia or incentive motivation impairment in depression and related disorders (78) or to dysphoria after lesions encroaching on the VP hotspot (79)(80)(81).…”

Section: Reward Component Separation By Population Segregation and Fimentioning

confidence: 99%

Disentangling pleasure from incentive salience and learning signals in brain reward circuitry

Smith

Berridge

Aldridge

2011

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

354

330

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Multiple signals for reward-hedonic impact, motivation, and learned associative prediction-are funneled through brain mesocorticolimbic circuits involving the nucleus accumbens and ventral pallidum. Here, we show how the hedonic "liking" and motivation "wanting" signals for a sweet reward are distinctly modulated and tracked in this circuit separately from signals for Pavlovian predictions (learning). Animals first learned to associate a fixed sequence of Pavlovian cues with sucrose reward. Subsequent intraaccumbens microinjections of an opioid-stimulating drug increased the hedonic liking impact of sucrose in behavior and firing signals of ventral pallidum neurons, and likewise, they increased incentive salience signals in firing to the reward-proximal incentive cue (but did not alter firing signals to the learned prediction value of a reward-distal cue). Microinjection of a dopamine-stimulating drug instead enhanced only the motivation component but did not alter hedonic impact or learned prediction signals. Different dedicated neuronal subpopulations in the ventral pallidum tracked signal enhancements for hedonic impact vs. incentive salience, and a faster firing pattern also distinguished incentive signals from slower hedonic signals, even for a third overlapping population. These results reveal separate neural representations of wanting, liking, and prediction components of the same reward within the nucleus accumbens to ventral pallidum segment of mesocorticolimbic circuitry.addiction | obesity | limbic | reinforcement | striatum

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Section: Reward Component Separation By Population Segregation and Fimentioning

confidence: 99%

Disentangling pleasure from incentive salience and learning signals in brain reward circuitry

Smith

Berridge

Aldridge

2011

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

354

330

View full text Add to dashboard Cite

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“…Striatal and cingulate lesions would potentially be associated with less riskaverse (and more risk neutral) choices. A striatal lesion could reduce the ability to evaluate magnitude, an effect that is also implied by negative motivational changes in patients with globus pallidus lesions (Vijayaraghavan et al, 2008). Nevertheless, such a lesion could be compensated by functions in other areas, namely ventromedial prefrontal cortex.…”

Section: Combined Bold Signals Contributing To Decision Makingmentioning

confidence: 99%

Neural Correlates of Value, Risk, and Risk Aversion Contributing to Decision Making under Risk

Christopoulos¹,

Tobler²,

Bossaerts³

et al. 2009

J. Neurosci.

389

323

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Decision making under risk is central to human behavior. Economic decision theory suggests that value, risk, and risk aversion influence choice behavior. Although previous studies identified neural correlates of decision parameters, the contribution of these correlates to actual choices is unknown. In two different experiments, participants chose between risky and safe options. We identified discrete blood oxygen level-dependent (BOLD) correlates of value and risk in the ventral striatum and anterior cingulate, respectively. Notably, increasing inferior frontal gyrus activity to low risk and safe options correlated with higher risk aversion. Importantly, the combination of these BOLD responses effectively decoded the behavioral choice. Striatal value and cingulate risk responses increased the probability of a risky choice, whereas inferior frontal gyrus responses showed the inverse relationship. These findings suggest that the BOLD correlates of decision factors are appropriate for an ideal observer to detect behavioral choices. More generally, these biological data contribute to the validity of the theoretical decision parameters for actual decisions under risk.

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“…Neurobiological studies have shown that lesions in reward and motivation circuits result in anhedonia [83,[98][99][100] with neuroimaging studies demonstrating decreased activation in the medial frontal cortex as a possible causative factor underlying abnormal positive affect processing in patients [101][102][103].…”

Section: Anhedoniamentioning

confidence: 99%

Hedonic Tone: A Bridge between the Psychobiology of Depression and its Comorbidities

A¹

2014

J Depress Anxiety

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paper will present the hypothesis that low hedonic tone and associated specific neurobiologic correlates predict the presence of ADHD in MDD, thus who is at risk for poorer outcomes with selective Serotonin Reuptake Inhibitors (SSRIs). Brain Regions and CircuitsEleven key areas of the brain have been highlighted in part by their specific neurotransmitter projections of which alteration in neurotransmitter innervation has been hypothesized to create disruptions in information processing and consequently specific psychological symptoms [2]. Linking each of these functional areas is a network of neuron projections or neurotransmitter pathways from the brainstem. It is posited that when a neurotransmitter-carrying neuron projects into a specific area, it has the capacity to modulate the physiological processes of the associated circuit [2]. Thus these pathways form the substrates that "tune" the neurons within each AbstractTreatment of Major Depressive Disorder (MDD), in many cases, offers less than optimal results, resulting in loss of function and remaining impairment. This is partially explained by the high prevalence of comorbid psychiatric illnesses that share common features, likely resulting in less than adequate treatment outcomes among patients receiving traditional psychiatric treatment.The term anhedonia does not sufficiently capture the complex and multifaceted reward-associated deficits seen in neuropsychiatric disorders. Deficits in reward-related processes can lead to behaviors that may appear to be the loss of interest or pleasure, and may preclude an individual from engaging in goal-oriented action. Investigators have identified a lifelong poor hedonic responsiveness, manifested as altered sensitivity to reinforcement, in patients with Attention Deficit Hyperactivity Disorder (ADHD), and suggest it as a common endophenotype for depression and the inattentive symptoms of ADHD. Research into the neurobiology of anhedonia has focused on the centers in the brain related to reward and motivation, and has identified the dopaminergic and associated circuits as playing a key role. Studies have shown that lesions in reward and motivation circuits result in anhedonia, and that decreased activation in the medial frontal cortex is believed to underlie abnormal positive affect processing in patients.In this paper, we propose that a specific phenotype of depression, which is more likely to be described as "treatment resistant" is associated with high risk of comorbidity with dysthymia, ADHD, and substance abuse, specifically cocaine abuse. We believe these patients experience a chronically lower hedonic tone that results in chronic anhedonia (as opposed to acute state anhedonia noted in a major depressive episode) related to unique pathophysiology and requiring treatment of the dopaminergic deficiency that characterizes its unique collection of comorbidities.

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Emotional and motivational changes after bilateral lesions of the globus pallidus.

Cited by 38 publications

References 26 publications

Disentangling pleasure from incentive salience and learning signals in brain reward circuitry

Disentangling pleasure from incentive salience and learning signals in brain reward circuitry

Neural Correlates of Value, Risk, and Risk Aversion Contributing to Decision Making under Risk

Hedonic Tone: A Bridge between the Psychobiology of Depression and its Comorbidities

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