Fast-spiking inhibitory γ-aminobutyric acid (GABA) interneurons expressing the calcium-binding protein parvalbumin have been implicated in the mediation of gamma oscillatory activity (Carlen et al., 2011; Gonzalez-Burgos et al., 2010; Lewis et al., 2011; Sohal et al., 2009). The inhibition of pyramidal cell and interneuron networks by GABAergic interneurons produces gamma band oscillations through an inhibition and rebound excitation cycle that is modulated by GABAA receptors (Sohal et al., 2009; Whittington et al., 1995). Moreover, glutamatergic neurotransmission at NMDA receptors provides excitatory regulation of parvalbumin fast-spiking interneurons, contributing to the generation of gamma oscillations in pyramidal cell networks (Carlen et al., 2011; Doheny et al., 2000; Roopun et al., 2008). Gamma oscillatory activity non-invasively measured by EEG in patients with schizophrenia is of interest because disrupted GABAergic and glutamatergic cortical activity have been implicated in the pathophysiology of the illness (Benes, 2000; Gonzalez-Burgos and Lewis, 2008; Lewis et al., 2005; Lewis et al., 2011; Lewis et al., 2008; Roopun et al., 2008).
