Nicotine Enhances Visuospatial Attention by Deactivating Areas of the Resting Brain Default Network

Hahn, Britta; Ross, Thomas J.; Yang, Yihong; Kim, Insook; Huestis, Marilyn A.; Stein, Elliot A.

doi:10.1523/jneurosci.5129-06.2007

Cited by 187 publications

(199 citation statements)

References 62 publications

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“…First, nicotine, a cholinergic agonist, was found to improve response latency in cue-target detection tasks by enhancing the cognitive brain mechanisms specifically involved in conditions where no extrinsic cue is provided [74,75]. Consistent with our results, the benefit in response latency was found to rely on the deactivation of the default activity of the dorsomedian frontal cortex, the precuneus and the PCC [75,76]. Second, the design used in this study was adapted from a classical task well known to engage the locus coeruleusnorepinephrine network [77][78][79][80].…”

Section: Relevance To the Neurochemical Bases Of Akinesiasupporting

confidence: 88%

Deep Brain Stimulation of the Subthalamic Nucleus, but not Dopaminergic Medication, Improves Proactive Inhibitory Control of Movement Initiation in Parkinson's Disease

et al. 2013

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Slowness in movement initiation is a cardinal feature of Parkinson's disease (PD) that is still poorly understood and unsuccessfully alleviated by standard therapies. Here, we raise this major clinical issue within the framework of a novel theoretical model that allows a better understanding of the basic mechanisms involved in movement initiation. This model assumes that movement triggering is inhibited by default to prevent automatic responses to unpredictable events. We investigated to which extent the top-down control necessary to release this locking state before initiating actions is impaired in PD and restored by standard therapies. We used a cue-target reaction time task to test both the ability to initiate fast responses to targets and the ability to refrain from reacting to cues. Fourteen patients with dopaminergic (DA) medication and 11 with subthalamic nucleus (STN) stimulation were tested on and off treatment, and compared with 14 healthy controls. We found evidence that patients withdrawn from treatment have trouble voluntarily releasing proactive inhibitory control; while DA medication broadly reduces movement initiation latency, it does not reinstate a normal pattern of movement initiation; and stimulation of the STN specifically re-establishes the efficiency of the top-down control of proactive inhibition. These results suggest that movement initiation disorders that resist DA medication are due to executive, not motor, dysfunctions. This conclusion is discussed with regard to the role the STN may play as an interface between non-DA executive and DA motor systems in cortico-basal ganglia loops.

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Section: Relevance To the Neurochemical Bases Of Akinesiasupporting

confidence: 88%

Deep Brain Stimulation of the Subthalamic Nucleus, but not Dopaminergic Medication, Improves Proactive Inhibitory Control of Movement Initiation in Parkinson's Disease

et al. 2013

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“…DMN deactivation has been linked to successful performance in cognitive tasks (Anticevic et al, 2010;Hahn et al, 2007), whereas failure of DMN deactivation during verbal WM has been observed in schizophrenia (Matsuo et al, 2013). Functional connectivity changes in DMN have also been reported in schizophrenia patients and their first-degree relatives (Garrity et al, 2007;Whitfield-Gabrieli et al, 2009).…”

Section: Limbic and Default Vmpfc And Their Relation To Performance Imentioning

confidence: 99%

Disrupted Working Memory Circuitry in Schizophrenia: Disentangling fMRI Markers of Core Pathology vs Other Aspects of Impaired Performance

Eryilmaz

Tanner

et al. 2016

Neuropsychopharmacol

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Working memory (WM) impairment, a core feature of schizophrenia, is often associated with aberrant dorsolateral prefrontal cortex (dlPFC) activation. Reduced resting-state connectivity within the frontoparietal control network (FPCN) has also been reported in schizophrenia. However, interpretation of WM-related dlPFC dysfunction has been limited by performance differences between patients and controls, and by uncertainty over the relevance of resting-state connectivity to network engagement during task. We contrasted brain activation in 40 schizophrenia patients and 40 controls during verbal WM performance, and evaluated underlying functional connectivity during rest and task. During correct trials, patients demonstrated normal FPCN activation, despite an inverse relationship between positive symptoms and activation. FPCN activation differed between the groups only during error trials (controls4patients). In contrast, controls demonstrated stronger deactivation of the ventromedial prefrontal cortex (vmPFC) during correct and error trials. Functional connectivity analysis indicated impaired resting-state FPCN connectivity in patients, but normal connectivity during task. However, patients showed abnormal connectivity among regions such as vmPFC, lateral orbitofrontal cortex, and parahippocampal gyrus (PHG) during both rest and task. During task, patients also exhibited altered thalamic connectivity to PHG and FPCN. Activation and connectivity patterns that were more characteristic of controls generally correlated with better performance. In summary, patients demonstrated normal FPCN activation when they remained on-task, and exhibited normal FPCN connectivity during WM, whereas vmPFC deactivation differences persisted regardless of WM performance. Our findings suggest that altered FPCN activation in patients reflects performance difference, and that limbic and thalamic dysfunction is critically involved in WM deficits in schizophrenia.

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“…In contrast, the control subjects deactivated some of these regions (PostCG5), consistent with similar deactivations during a large variety of other cognitive tasks as previously reported (Raichle ME et al, 2001). In general, task-related deactivations of brain regions have been associated with the temporary suspension of the baseline state (default mode) of brain function, and may be crucial for accurate performance on cognitive tasks (Hahn B, TJ et al, 2007;Raichle ME et al, 2001). Indeed, the inability to deactivate the PostCG in the cocaine subjects compared to control subjects may have contributed to the lower accuracy in the former group during the 2-back task.…”

Section: Hyperactivationmentioning

confidence: 99%

Widespread disruption in brain activation patterns to a working memory task during cocaine abstinence

et al. 2007

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Cocaine abstinence is associated with impaired performance in cognitive functions including attention, vigilance and executive function. Here we test the hypothesis that cognitive dysfunction during cocaine abstinence reflects in part impairment of cortical and subcortical regions modulated by dopamine. We used functional magnetic resonance imaging (fMRI) to study brain activation to a verbal working memory task in cocaine abusers (n = 16) and healthy controls (n = 16). Compared to controls, cocaine abusers showed: (1) hypoactivation in the mesencephalon, where dopamine neurons are located, as well as the thalamus, a brain region involved in arousal; (2) larger deactivation in dopamine projection regions (putamen, anterior cingulate, parahippocampal gyrus, and amygdala); and (3) hyperactivation in cortical regions involved with attention (prefrontal and parietal cortices), which probably reflects increased attention and control processes as compensatory mechanisms. Furthermore, the working memory load activation was lower in the prefrontal and parietal cortices in cocaine abusers when compared with controls, which might reflect limited network capacity. These abnormalities were accentuated in the cocaine abusers with positive urines for cocaine at time of study (as compared to cocaine abusers with negative urines) suggesting that the deficits may reflect in part early cocaine abstinence. These findings provide evidence of impaired function of regions involved with executive control, attention and vigilance in cocaine abusers. This widespread neurofunctional disruption is likely to underlie the cognitive deficits during early cocaine abstinence, and to reflect involvement of dopamine as well as other neurotransmitters.

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Nicotine Enhances Visuospatial Attention by Deactivating Areas of the Resting Brain Default Network

Cited by 187 publications

References 62 publications

Deep Brain Stimulation of the Subthalamic Nucleus, but not Dopaminergic Medication, Improves Proactive Inhibitory Control of Movement Initiation in Parkinson's Disease

Deep Brain Stimulation of the Subthalamic Nucleus, but not Dopaminergic Medication, Improves Proactive Inhibitory Control of Movement Initiation in Parkinson's Disease

Disrupted Working Memory Circuitry in Schizophrenia: Disentangling fMRI Markers of Core Pathology vs Other Aspects of Impaired Performance

Widespread disruption in brain activation patterns to a working memory task during cocaine abstinence

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