have found evidence for generators of novelty P3 in multiple areas, including frontal and posterior association cortex, hippocampus and anterior cingulate cortex (Halgren et al., 1995). ERP studies using source localization techniques have localized generators of novelty P3 to anterior cingulate, whereas the P3b to target stimuli has sources in the region of the temporal–parietal junction (Dien et al., 2003; Mecklinger and Ullsperger, 1995). Focal lesions in the posterior hippocampal region also result in reduction of novelty P3a particularly over prefrontal regions, whereas posterior P3b amplitude to targets is unaffected by hippocampal damage (Knight, 1996). This led Knight et al. (1998) to conclude that a distributed frontal-hippocampal system is involved in novelty processing. The P3 novelty reduction in depressed patients may therefore involve dysfunction of a distributed network, including prefrontal, anterior cingulate, and hippocampal regions.
