Abstract
Recent advances in electroneurophysiology (EEG/MEG, Optogenetics) and postmortem studies have revealed that cortical neural oscillation deficit play critical roles in the pathophysiology of schizophrenia. A growing body of evidence is accumulating to show that such synchronous oscillations especially within the γband which relates to perception, cognition and consciousness, exhibit deficits in schizophrenia. Impairments in γband oscillation have been hypothesized to arise from disruption of GABAergic inhibitory interneuron one act as a rhythm maker in neural circuit, and excitatory neuron (NMDAR hypofunction), as well as abnormal neuronal balance of excitation and inhibition (E/I balance). Moreover, these phenomena are believed to be observed across species and can be obtained from animal models of schizophrenia. Thus, γ band oscillation deficit have attracted a lot of attention as a new pathophysiological model of schizophrenia and its therapeutic target.
