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Nee, D. E.

Publications and source records attributed to Nee, D. E..

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Correspondence: fMRI replicability depends upon sufficient individual-level data

The replicability of findings drawn from functional magnetic resonance imaging (fMRI) data have increasingly been called into question. Concerns have been raised that historically, sample sizes have been insufficient to produce adequate power, leading to unreliable results. Recently, Turner and colleagues demonstrated that even with large sample sizes, the replicability of fMRI can be worryingly low. However, their datasets featured low amounts of data at the individual-level. Here, I demonstrate that replicability depends critically on sufficient individual-level sampling. I show that fMRI can have strong replicability even at modest sample sizes when individuals are adequately sampled, but that inadequate individual-level sampling leads to poor replicability. These data indicate that fMRI replicability cannot be judged solely on sample size, and that adequate sampling at the individual-level is a critical design consideration.

neuroscience

Causal Evidence for Lateral Prefrontal Cortex Dynamics Supporting Cognitive Control

The lateral prefrontal cortex (LPFC) is essential for higher-level cognition, but how interactions among LPFC areas support cognitive control has remained elusive. In previous work, dynamic causal modeling (DCM) of fMRI data revealed that demands on cognitive control elicited a convergence of influences towards mid LPFC. We proposed that these findings reflect the integration of abstract, rostral and concrete, caudal influences to inform context-appropriate action. Here, we provide a causal test of this model using continuous theta-burst transcranial magnetic stimulation (cTBS). cTBS was applied to caudal, mid, or rostral LPFC, as well as a control site in counterbalanced sessions. In most cases, behavioral modulations resulting from cTBS could be predicted based upon the direction of influences within the previously estimated DCM. However, inconsistent with our DCM, we found that cTBS to caudal LPFC impaired cognitive control processes presumed to involve rostral LPFC. Revising the original DCM with a pathway from caudal LPFC to rostral LPFC significantly improved the fitted DCM and accounted for the observed behavioral findings. These data provide causal evidence for LPFC dynamics supporting cognitive control and demonstrate the utility of combining DCM with causal manipulations to create, test, and refine models of cognition.

neuroscience