Abstract
While a large body of literature documents the impairing effect of anxiety on cognition, performing a demanding task was shown to be effective in reducing anxiety. Here we explored the mechanisms of this anxiolytic effect by examining how a pharmacological challenge designed to improve attentional processes influences the interplay between the neural networks engaged during anxiety and cognition. Using a double-blind between-subject design, we pharmacologically manipulated working memory (WM) using a single oral dose of 20 mg methylphenidate (MPH, cognitive enhancer) or placebo. Fifty healthy adults (25/drug group) performed two runs of a WM N-back task in a 3 T magnetic resonance imaging scanner. This task comprised a low (1-Back) and high (3-Back) WM load, which were performed in two contexts, safety or threat of shocks (induced-anxiety). Analyses revealed that (1) WM accuracy was overall improved by MPH and (2) MPH (vs. placebo) strengthened the engagement of regions within the fronto-parietal control network (FPCN) and reduced the default mode network (DMN) deactivation. These MPH effects predominated in the most difficult context, i.e., threat condition, first run (novelty of the task), and 3-Back task. The facilitation of neural activation can be interpreted as an expansion of cognitive resources, which could foster both the representation and integration of anxiety-provoking stimuli as well as the top–down regulatory processes to protect against the detrimental effect of anxiety. This mechanism might establish an optimal balance between FPCN (cognitive processing) and DMN (emotion regulation) recruitment.
Highlights
While a large body of literature documents the impairing effect of anxiety on cognition [for reviews, see [1,2,3,4], performing a demanding task was shown to be effective in reducing anxiety [5,6,7,8,9,10]
MPH was associated with stronger physiological responses to anxiety. These findings suggested that cognitive resources could be used to both foster the engagement of cognitive capacity and to process anxiety-provoking stimuli and associated defensive responses
A MPH-driven increase in the dissociation between the engagement of the FPCN and DMN as reflected by (i) stronger activation of fronto-parietal control network (FPCN) regions, which favors cognitive performance and (ii) steeper deactivation of default mode network (DMN) regions, which prevents interference from irrelevant stimuli such as anxiety-related signals
Summary
While a large body of literature documents the impairing effect of anxiety on cognition [for reviews, see [1,2,3,4], performing a demanding task was shown to be effective in reducing anxiety [5,6,7,8,9,10] This neuroimaging study examines potential neural mechanisms underlying this effect that could be exploited in the treatment of anxiety. To this aim, a pharmacological manipulation of cognitive function using a cognitive enhancer (methylphenidate (MPH)) was designed to investigate the interaction of induced-anxiety with performance on a working memory (WM) task. The most common effects of anxiety on neural networks, evidenced by resting-state neuroimaging studies, are of two types: (1) an impaired functional
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