All of these processes interact in a complex way. Nonetheless, in experimentally well controlled tasks, some of these variables can be varied, whereas others can be kept constant. The experimental
variation of attentional processes is a typical characteristic of tasks that are used to investigate the P1. Spatial cuing paradigms are a good example. According to our hypotheses, two different processes, T and S are of primary importance in this type of tasks. In type 1 tasks, T is experimentally manipulated by instructing subjects to attend to the left or right hemifield. In type 2 tasks, T is varied by the cue and its validity. T establishes a top–down control process that operates to increase SNR in task relevant networks. In contrast, S is a process that blocks information Nintedanib concentration processing in interfering networks. Thus, attentional benefits – associated with the influence of T – and attentional costs – associated with the influence of S – are both due to an increase in inhibition which leads to an increase in P1 amplitude. The difference between T and S is seen in different inhibitory processes that operate in task relevant vs. interfering networks (cf. Fig. 5A). Attentional processes are not the only class of cognitive processes that affect the P1 component. Processing complexity (C) during early stimulus Z-VAD-FMK categorization is another important
cognitive process that shapes the P1. As an example, orthographic neighborhood size (N), and word length may be considered variables that directly affect C. A pop-out color target search may be considered an example affecting D, the focused Rucaparib search for a complex target lacking pop-out features may be considered an example affecting primarily T, whereas the processing of a distractor item may be considered an example for S. In this section we apply the proposed theory particularly to those findings which are difficult to interpret in terms of stimulus evoked activity
or on the basis of an enhancement hypothesis. An overview over the findings reviewed in Section 2 and their interpretation on the basis of the P1 inhibition timing hypothesis are presented in Fig. 5B. The central prediction of the proposed theory rests on inhibition and on the idea that suppression of task irrelevant and potentially competing information and or neural structures leads to a particularly large increase in the P1 amplitude. Under controlled conditions this suppression related increase will be at least as large or larger than for task relevant processes where inhibition is used to increase the SNR. As a first example let us consider the finding of a large ipsilateral P1 amplitude. We assume that the increased ipsilateral P1 reflects inhibition of task irrelevant and potentially competing processes.