Abstract
Much of the mechanistic research on anxiety focuses on subcortical structures such as the amygdala; however, less is known about the distributed cortical circuit that also contributes to anxiety expression. One way to learn about this circuit is to probe candidate regions using transcranial magnetic stimulation (TMS). In this study, we tested the involvement of the dorsolateral prefrontal cortex (dlPFC), in anxiety expression using 10 Hz repetitive TMS (rTMS). In a within-subject, crossover experiment, the study measured anxiety in healthy subjects before and after a session of 10 Hz rTMS to the right dorsolateral prefrontal cortex (dlPFC). It used threat of predictable and unpredictable shock to induce anxiety and anxiety potentiated startle to assess anxiety. Counter to our hypotheses, results showed an increase in anxiety-potentiated startle following active but not sham rTMS. These results suggest a mechanistic link between right dlPFC activity and physiological anxiety expression. This result supports current models of prefrontal asymmetry in affect, and lays the groundwork for further exploration into the cortical mechanisms mediating anxiety, which may lead to novel anxiety treatments.
Highlights
The bulk of the mechanistic research into anxiety expression implicates sub-cortical structures such as the amygdala and bed nucleus of the stria terminalis; [1] there exists a large body of literature implicating large-scale brain networks in anxiety [2]
BOLD responses in the dorsolateral prefrontal cortex (dlPFC) during threat are negatively correlated with subjective anxiety [6], tasks that activate the dlPFC reduce anxiety potentiated startle (APS), and dlPFC activity during threat positively correlates with performance when task demands are high [7]
We identified the BOLD peak within the right dlPFC, which was defined using a group-level functional ROI from a previous study using the same Sternberg Working Memory (WM) task (See Fig. 2a) aligned to native space
Summary
The bulk of the mechanistic research into anxiety expression implicates sub-cortical structures such as the amygdala and bed nucleus of the stria terminalis; [1] there exists a large body of literature implicating large-scale brain networks in anxiety [2]. BOLD responses in the dlPFC during threat are negatively correlated with subjective anxiety [6], tasks that activate the dlPFC reduce anxiety potentiated startle (APS), and dlPFC activity during threat positively correlates with performance when task demands are high [7]. Together these results suggest that facilitating dlPFC activity should reduce anxiety; this is not reflected in the current therapeutic application of rTMS to treat anxiety symptoms in depression [8]. This type of application is consistent with the interpretation that the right dlPFC is important for anxiety expression rather than regulation [9], but inconsistent with our previous results
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