The left dorsal stream causally mediates the tone labeling in absolute pitch

Absolute pitch (AP) refers to the ability to effortlessly identify given pitches without any reference. Correlative evidence suggests that the left posterior dorsolateral prefrontal cortex (DLPFC) is responsible for the process underlying pitch labeling in AP. Here, we measured the sight‐reading performance of right‐handed AP possessors and matched controls under cathodal and sham transcranial direct current stimulation of the left DLPFC. The participants were instructed to report notations as accurately and as fast as possible by playing with their right hand on a piano. The notations were simultaneously presented with distracting auditory stimuli that either matched or mismatched them in different semitone degrees. Unlike the controls, AP possessors revealed an interference effect in that they responded slower in mismatching conditions than in the matching one. Under cathodal stimulation, this interference effect disappeared. These findings confirm that the pitch‐labeling process underlying AP occurs automatically and is largely nonsuppressible when triggered by tone exposure. The improvement of the AP possessors’ sight‐reading performances in response to the suppression of the left DLPFC using cathodal stimulation confirms a causal relationship between this brain structure and pitch labeling. By applying a cathodal‐sham tDCS protocol, we provided, for the first time, causal evidence that the left dorsolateral prefrontal cortex (DLPFC) drives the pitch‐labeling process underlying absolute pitch (AP). Furthermore, the findings yielded from our customized piano‐playing Stroop task support automaticity as a unique feature of AP, confirming a unique pitch‐processing mode virtually nonreliant on cognitive load. Altogether, these findings substantiate previous functional studies showing that AP possessors selectively recruit the left DLPFC during tone exposure and label tones without relying on working memory resources, as discussed with reference to reduced or absent P3 responses and lack of activation in the inferior frontal gyrus.