The causal role of DLPFC top-down control on the acquisition and the automatic expression of implicit learning: State of the art

Implicit learning refers to the incidental acquisition and expression of knowledge that is not accompanied by full awareness of its contents. Implicit sequence learning (ISL) represents one of the most useful paradigms to investigate these processes. In this paradigm, participants are usually instructed to respond to the location of a target that moves regularly through a set of possible locations. Although participants are not informed about the existence of a sequence, they eventually learn it implicitly, as attested by the costs observed when this sequence is violated in a reduced set of control trials. Interestingly, the expression of this learning decreases immediately after a control trial, in a way that resembles the adjustments triggered in response to incongruent trials in interference tasks. These effects have been attributed to a control network involving dorsolateral prefrontal cortex (DLPFC) and cingulate (ACC) structures. In the present work, we reviewed a group of recent studies which had inhibited DLPFC top-down control by means of non-invasive brain stimulation to increase the acquisition of ISL. In addition, as no previous study has investigated the effect of inhibiting top-down control on releasing the automatic expression of ISL, we present a pre-registered – yet exploratory – study in which an inhibitory continuous theta burst stimulation protocol was applied over an anterior-ventral portion of the dorsolateral prefrontal cortex (DLPFC) highly interconnected with the ACC, and whose activity has been specifically linked to motor control (i.e., Right DLPFC, n = 10 or the Left DLPFC, n = 10), compared to active Vertex stimulation (n = 10). Contrary to our hypotheses, the results did not show evidence for the involvement of such region in the expression of ISL. We discussed the results in the context of the set of contradictory findings reported in the systematic review.