Our results support EAGBR measures as putative endophenotypes of schizophrenia, likely reflecting an ubiquitous local cortical circuit deficit.

These results suggest that ERO deficits in gamma to S1 and beta to S2 stimuli and impaired ERO gating are associated with SZ, but are not related to genetic liability for the illness. The components of information processing assessed by gamma- and beta gating appear to be independent from those mediated by P50 suppression.

No abstract