Background: The P50 event-related potential sensory gating deficit, a failure to inhibit responses to repeated stimuli, is a leading endophenotype for schizophrenia (SZ). Both gamma and beta event-related oscillations (EROs) are major contributors to the auditory P50 response. However, the topographic distribution of gamma and beta ERO responses to initial (S1) and repeat (S2) stimuli and the association of these oscillations with P50 sensory gating are not clear.
Methods: A total of 51 schizophrenic patients, 25 unaffected first-degree relatives, and 34 healthy comparison subjects were tested using a paired-click paradigm. Evoked power of gamma- and beta-band responses using wavelet analyses to S1 and S2 stimuli and gating of EROs and P50 were the main outcome measures.
Results: A P50 gating deficit was found in patients (P < .001) and at a trend level in relatives (P = .087). Patients showed widely distributed reductions in gamma and beta EROs to S1 stimuli and S2 stimuli, respectively, and impaired gating in both frequencies. Reduced gamma and beta ERO activity in patients was associated primarily with age of onset. Relatives did not differ significantly from control subjects in either EROs power or gating. Gating of P50, gamma, and beta were not significantly correlated (r = .18-.19, P > .05).
Conclusions: 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.