Most interestingly, however, this finding not only is obtained for recording sites over the contralateral, but also for the ipsilateral hemisphere. As is evident from Fig. 1B, the P1 is primarily modulated by attention and not by stimulus presentation. The attended hemisphere (see the ‘attend’ condition in Fig. 1B) shows a general larger P1, regardless whether this hemisphere receives a stimulus (contralateral, attend) or not (ipsilateral, attend). This fact is also manifested statistically as a main effect for attention (at temporo-parietal sites) with

an absence of significant interactions with hemifield of presentation and hemisphere of recording for the P1. The important finding here is the large ipsilateral P1 and the Smad2 phosphorylation fact that the P1 is modulated by attention in the ipsilateral hemisphere in the same way as in the contralateral hemispheres. We argue that this finding suggests an inhibitory function of the P1 and conflicts with

traditional interpretations. For the sake of clarity, we distinguish between three different hypotheses, which we term the (i) baseline, (ii) stimulus enhancement (or evoked), and (iii) inhibition hypothesis. The baseline hypothesis was suggested by Hillyard Silmitasertib molecular weight et al., 1998, Luck et al., 1994 and Luck and Hillyard, 1995. The idea here is that relative to a neutral baseline (e.g., relative to a neutral cue) the P1 is not increased by attention, but suppressed in the unattended condition. This interpretation is interesting because it also assumes an inhibitory function of the P1 but in the sense that inhibition reduces the P1 amplitude. Or in other words, if irrelevant information must be suppressed, the P1 will be smaller as compared to a case where attention is focused on relevant Nutlin-3 cell line information. The stimulus enhancement or evoked hypothesis predicts

that the P1 is enlarged if the processing of a stimulus (which evokes an ERP-component) is enhanced by attention. If a stimulus is not attended, it still will elicit an evoked component, but the component will be smaller as compared to attended stimuli. The inhibition hypothesis – which will be introduced below – assumes that the P1 reflects inhibitory processes that have different functions in task relevant and task irrelevant neural structures. In the former, inhibition operates to increase the signal to noise ratio (SNR), in the latter inhibition operates to block information processing. The central prediction here is that inhibition increases the P1. The question, in which way inhibition shapes the P1 amplitude in task relevant and irrelevant neuronal structures is discussed in detail in Section 3. The critical point now is the claim that the baseline and enhancement hypotheses will not be able to explain why a large P1 is generated at ipsilateral recording sites. Both interpretations appear plausible to explain the findings for the contra- but not those observed for the ipsilateral hemisphere.