A multitude of neurophysiologic abnormalities have been documented in schizophrenia (e.g., Luck et al., 2011), some of which may potentially be used as translational biomarkers for drug discovery (e.g., Javitt et al., 2008). These abnormalities include electroencephalography (EEG) measures obtained in the time domain, notably event-related potentials (ERPs) that index neuronal functions ranging from early sensory (e.g., P1, N1) to late cognitive (e.g., P3) processing, or in the frequency domain, including power spectra that index attentional control (e.g., alpha) or binding of perceptual features (e.g., gamma). Initially, high expectations had been placed in the almost ubiquitous reduction of P3 amplitude, which has been associated with negative symptoms and may serve both as a state and trait marker of schizophrenia (e.g., Mathalon et al., 2000); however, a decrease in P3 amplitude is not specific to the disorder and is often observed, for example, in alcoholism, depression, bipolar disorder, or Alzheimer’s disease (e.g., Ford, 1999). Still, P3 reductions and other neurophysiologic deficits have also been observed in unaffected relatives and first-episode patients (e.g., Bramon et al., 2005; Ford, 1999; Hirayasu et al.,
