in the early stages and a decreased in chronic patients. Moreover, a recent meta-analysis showed greater age-dependent decrease in glutamate and glutamine concentration in schizophrenia compared to controls (Marsman et al., 2013). Our findings have interesting similarities with those from studies of animal models of psychoses that showed increased gamma oscillations after acute administration of ketamine (Pinault, 2008) and decrease after chronic administration (McNally et al., 2013). Recent studies have contributed to better understand the role of gamma oscillations in human brain function (Buzsaki and Wang, 2012) and its implications in schizophrenia (Sun et al., 2011; Uhlhaas, 2011; Uhlhaas and Singer, 2013). In particular, GABAergic interneurons with glutamate regulating effect through N-methyl-D-aspartate (NMDA) receptors have been postulated to be responsible for the dysfunction of gamma oscillations observed in schizophrenia (Spencer, 2009; Gonzalez-Burgos and Lewis, 2012). Finally, as showed in basic (Kocsis et al., 2014), computational (Komek et al., 2012; Wang and Wong-Lin, 2013) and human studies (Demiralp et al., 2007; Komek et al., 2012) a relevant role in the generating and modulating gamma activity, via regulation of GABAergic (Andersson et al., 2012b) and glutamatergic transmission (Andersson et al., 2012a), is also played by dopamine (Herrmann and Demiralp, 2005; Furth et
