Excitotoxic lesions of the core and shell subregions of the nucleus accumbens differentially disrupt body weight regulation and motor activity in rat

Cs, Maldonado-Irizarry; Kelley, Ann E.

doi:10.1016/0361-9230(95)02030-2

Cited by 86 publications

(47 citation statements)

References 40 publications

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“…AcbC lesions also reduced efficiency (the number of responses made per reward earned) in a differential-reinforcement-oflow-rates (DRL) schedule (Pothuizen et al, 2005), in which animals must respond below a certain rate in order to obtain reward. This is much like the effects of whole-Acb lesions (Reading & Dunnett, 1995), although the DRL task may also be susceptible to general levels of motor activity: AcbC-lesioned rats are hyperactive Cardinal et al, 2001;Maldonado-Irizarry & Kelley, 1995;Parkinson, Olmstead, Burns, Robbins, & Everitt, 1999), and hyperactivity would itself tend to reduce DRL efficiency.…”

Section: Choice Involving Delayed Reinforcementmentioning

confidence: 99%

“…Furthermore, delay discounting and probability discounting may also reflect separate processes contributing to the selection of outcomes, as discussed above. Damage to the AcbC can produce impulsive choice, an impaired ability to choose delayed rewards Pothuizen et al, 2005), in addition to hyperactivity Cardinal et al, 2001;Maldonado-Irizarry & Kelley, 1995;Parkinson, Olmstead, et al, 1999), though without impairments in attentional function (Christakou, Robbins, & Everitt, 2004;Cole & Robbins, 1989) and without motoric impulsivity as assessed by the stop-signal task (Eagle & Robbins, 2003). Destruction of the AcbC does not, therefore, mimic all the signs of ADHD, but these findings suggest that the behaviour of rats with AcbC damage resembles that of humans with the hyperactive-impulsive subtype of ADHD (APA, 2000).…”

Section: Integration Of Acbc Functions With Respect To Impulsivitymentioning

confidence: 99%

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Neural systems implicated in delayed and probabilistic reinforcement

2006

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This review considers the theoretical problems facing agents that must learn and choose on the basis of reward or reinforcement that is uncertain or delayed, in implicit or procedural (stimulus-response) representational systems and in explicit or declarative (action-outcome-value) representational systems. Individual differences in sensitivity to delays and uncertainty may contribute to impulsivity and risk taking. Learning and choice with delayed and uncertain reinforcement are related but in some cases dissociable processes. The contributions to delay and uncertainty discounting of neuromodulators including serotonin, dopamine, and noradrenaline, and of specific neural structures including the nucleus accumbens core, nucleus accumbens shell, orbitofrontal cortex, basolateral amygdala, anterior cingulate cortex, medial prefrontal (prelimbic/infralimbic) cortex, insula, subthalamic nucleus, and hippocampus are examined.

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Section: Choice Involving Delayed Reinforcementmentioning

confidence: 99%

Section: Integration Of Acbc Functions With Respect To Impulsivitymentioning

confidence: 99%

Neural systems implicated in delayed and probabilistic reinforcement

2006

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“…25 In monkeys, the NA shell is more sensitive to novel circumstances and more involved in visceral and motivational mechanisms 26,27 than the NA core, which is involved specifically in motor control and the learning of appetitive behavioral responses. 28,29 Considering these functional roles in the caudate and NA, neuronal activation of these nuclei likely affects motor performance.…”

Section: Role Of the Mesolimbocortical Dopaminergic Pathwaymentioning

confidence: 99%

Effect of Subthalamic Nucleus Stimulation during Exercise on the Mesolimbocortical Dopaminergic Region in Parkinson'S Disease: A Positron Emission Tomography Study

Nozaki

Sugiyama

Yagi

et al. 2012

J Cereb Blood Flow Metab

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To elucidate the dynamic effects of deep brain stimulation (DBS) in the subthalamic nucleus (STN) during activity on the dopaminergic system, 12 PD patients who had STN-DBS operations at least 1 month prior, underwent two positron emission tomography scans during right-foot movement in DBS-off and DBS-on conditions. To quantify motor performance changes, the motion speed and mobility angle of the foot at the ankle were measured twice. Estimations of the binding potential of [ 11 C]raclopride (BP ND ) were based on the Logan plot method. Significant motor recovery was found in the DBS-on condition. The STN-DBS during exercise significantly reduced the [ 11 C]raclopride BP ND in the caudate and the nucleus accumbens (NA), but not in the dorsal or ventral putamen. The magnitude of dopamine release in the NA correlated negatively with the magnitude of motor load, indicating that STN-DBS facilitated motor behavior more smoothly and at less expense to dopamine neurons in the region. The lack of dopamine release in the putamen and the significant dopamine release in the ventromedial striatum by STN-DBS during exercise indicated dopaminergic activation occurring in the motivational circuit during action, suggesting a compensatory functional activation of the motor loop from the nonmotor to the motor loop system.

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“…N-methyl-d-aspartate lesions of the NAc core induced weight loss in rats, whereas the shell-lesion group gained weight. 66 The authors of the study argued that the loss of weight in the core group was due to changes in motor function given the core's connections to the extrapyramidal system. 29 It is conceivable that the core and shell have opposing effects on ingestive behavior, explaining the lack of any change in weight with large, nonspecific excitotoxic lesions encompassing both regions of the NAc.…”

Section: Evidence From Lesion Studiesmentioning

confidence: 99%

Deep brain stimulation in the treatment of obesity

Halpern¹,

Wolf²,

Bale

et al. 2008

JNS

141

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Obesity is a growing global health problem frequently intractable to current treatment options. Recent evidence suggests that deep brain stimulation (DBS) may be effective and safe in the management of various, refractory neuropsychiatric disorders, including obesity. The authors review the literature implicating various neural regions in the pathophysiology of obesity, as well as the evidence supporting these regions as targets for DBS, in order to explore the therapeutic promise of DBS in obesity.The lateral hypothalamus and ventromedial hypothalamus are the appetite and satiety centers in the brain, respectively. Substantial data support targeting these regions with DBS for the purpose of appetite suppression and weight loss. However, reward sensation associated with highly caloric food has been implicated in overconsumption as well as obesity, and may in part explain the failure rates of conservative management and bariatric surgery. Thus, regions of the brain's reward circuitry, such as the nucleus accumbens, are promising alternatives for DBS in obesity control.The authors conclude that deep brain stimulation should be strongly considered as a promising therapeutic option for patients suffering from refractory obesity. 625Abbreviations used in this paper: BMI = body mass index; DBS = deep brain stimulation; GABA = γ-aminobutyric acid; LH = lateral hypothalamus; MCH = melanin-concentrating hormone; NAc = nucleus accumbens; OCD = obsessive-compulsive disorder; PD = Parkinson disease; 6-OHDA = 6-hydroxydopamine; STN = subthalamic nucleus; VMH = ventromedial hypothalamus; VP = ventral pallidum.

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Excitotoxic lesions of the core and shell subregions of the nucleus accumbens differentially disrupt body weight regulation and motor activity in rat

Cited by 86 publications

References 40 publications

Neural systems implicated in delayed and probabilistic reinforcement

Neural systems implicated in delayed and probabilistic reinforcement

Effect of Subthalamic Nucleus Stimulation during Exercise on the Mesolimbocortical Dopaminergic Region in Parkinson'S Disease: A Positron Emission Tomography Study

Deep brain stimulation in the treatment of obesity

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