Article

Dopamine modulates default mode network deactivation in elderly individuals during the Tower of London task.

Montreal Neurological Institute, McGill University, Quebec, Canada.
Neuroscience Letters (Impact Factor: 2.03). 08/2009; 458(1):1-5. DOI: 10.1016/j.neulet.2009.04.025
Source: PubMed

ABSTRACT Task-induced deactivation is frequently reported in the ventro-medial prefrontal cortex (vmPFC) and posterior cingulate cortex (PCC), regions considered to belong to the default mode network. To investigate the effect of dopamine on task-induced deactivation, we used positron emission tomography to measure cerebral blood flow during performance of the Tower of London task before and after administration of the dopamine receptor agonist apomorphine in six healthy volunteers (49-66 years old) and six Parkinson disease patients (52-69 years old). Although task-induced deactivation was observed in the vmPFC and PCC in both groups and in both conditions, an inverse correlation between activation and problem complexity was observed in the vmPFC only in the apomorphine condition.

0 Bookmarks
 · 
142 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Existing evidence suggests that the presence of reward cues modifies the activity in attentional networks, however, the nature of these influences remains poorly understood. Here, we performed independent component analysis (ICA) in two fMRI datasets corresponding to two incentive delay tasks, which compared the response to reward (money and erotic pictures) and neutral cues, and yielded activations in the ventral striatum using a general linear model approach. Across both experiments, ICA revealed that both the right frontoparietal network and default mode network time courses were positively and negatively modulated by reward cues, respectively. Moreover, this dual neural response pattern was enhanced in individuals with strong reward sensitivity. Therefore, ICA may be a complementary tool to investigate the relevant role of attentional networks on reward processing, and to investigate reward sensitivity in normal and pathological populations.
    Brain Structure and Function 04/2014; · 7.84 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: A cardinal symptom of attention deficit and hyperactivity disorder (ADHD) is a general distractibility where children and adults shift their attentional focus to stimuli that are irrelevant to the ongoing behavior. This has been attributed to a deficit in dopaminergic signaling in cortico-striatal networks that regulate goal-directed behavior. Furthermore, recent imaging evidence points to an impairment of large scale, antagonistic brain networks that normally contribute to attentional engagement and disengagement, such as the task-positive networks and the default mode network (DMN). Related networks are the ventral attentional network (VAN) involved in attentional shifting, and the salience network (SN) related to task expectancy. Here we discuss the tonic-phasic dynamics of catecholaminergic signaling in the brain, and attempt to provide a link between this and the activities of the large-scale cortical networks that regulate behavior. More specifically, we propose that a disbalance of tonic catecholamine levels during task performance produces an emphasis of phasic signaling and increased excitability of the VAN, yielding distractibility symptoms. Likewise, immaturity of the SN may relate to abnormal tonic signaling and an incapacity to build up a proper executive system during task performance. We discuss different lines of evidence including pharmacology, brain imaging and electrophysiology, that are consistent with our proposal. Finally, restoring the pharmacodynamics of catecholaminergic signaling seems crucial to alleviate ADHD symptoms; however, the possibility is open to explore cognitive rehabilitation strategies to top-down modulate network dynamics compensating the pharmacological deficits.
    Frontiers in Psychology 01/2014; 5:183. · 2.80 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Parkinson's disease (PD) can result in cognitive impairment. Executive dysfunction often appears early, followed by more widespread deficits later in the course of the disease. Disruption of parallel basal ganglia thalamo-cortical loops that subserve motor and cognitive function has been described in PD. However, there is emerging evidence that the default mode network, a cortical network that is active at rest with reduced activation during task performance, may also play a role in disease related cognitive decline. Objective: To determine the relative contribution of the executive control and default mode networks to parkinsonian executive dysfunction in medicated non-demented patients. Methods: We used BOLD fMRI to measure resting state functional connectivity in the executive control and default mode (DM) networks, and examined switching, processing speed, working memory/attention and motor performance in 14 medicated non-demented PD participants and 20 controls. Results: Performance on neuropsychological measures was similar across groups. Functional connectivity was not different across disease conditions in the executive control network. DMN functional connectivity was decreased in the PD group, specifically between posterior cingulate, medial prefrontal, and inferior parietal nodes. Greater DMN functional connectivity was associated with faster processing speed in the PD group. Conclusions: The continuous relationship between DMN disconnection and executive task performance indicates a possible biological contributor to parkinsonian cognitive deficits. The dynamics of executive control network change may be different than that of the DMN, suggesting less sensitivity to early cognitive deficits.
    Journal of Parkinson's disease. 03/2014;