information about the potential response hand” (p. 1668). In the same study, the N2 component in NoGo trials was not modulated as a function of response priming. The authors have speculated that a modulation of the N2 inhibition component in NoGo trials is dependent on the occurrence of LRP activity. Nevertheless, on the basis of their findings that there was a difference in the N2 amplitudes between Go and NoGo trials, the authors have suggested that the presence of LRP activity in NoGo trials is not a requisite to replicate the traditional Go/NoGo effect. Therefore, their results suggest that a modulation in the N2 is due to activation in response to Go stimuli, rather than a modulation due to inhibition in response to NoGo stimuli.
