Gamma band oscillations: a key to understanding schizophrenia symptoms and neural circuit abnormalities

Purpose of review We review our current understanding of abnormal gamma band oscillations in schizophrenia, their association with symptoms and the underlying cortical circuit abnormality, with a particular focus on the role of fast-spiking parvalbumin gamma-aminobutyric acid (GABA) neurons in the disease state. Recent findings Clinical electrophysiological studies of schizophrenia patients and pharmacological models of the disorder show an increase in spontaneous gamma band activity (not stimulus-evoked) measures. These findings provide a crucial link between preclinical and clinical work examining the role of gamma band activity in schizophrenia. MRI-based experiments measuring cortical GABA provides evidence supporting impaired GABAergic neurotransmission in schizophrenia patients, which is correlated with gamma band activity level. Several studies suggest that stimulation of the cortical circuitry, directly or via subcortical structures, has the potential to modulate cortical gamma activity, and improve cognitive function. Abnormal gamma band activity is observed in patients with schizophrenia and disease models in animals, and is suggested to underlie the psychosis and cognitive/perceptual deficits. Convergent evidence from both clinical and preclinical studies suggest the central factor in gamma band abnormalities is impaired GABAergic neurotransmission, particularly in a subclass of neurons which express parvalbumin. Rescue of gamma band abnormalities presents an intriguing option for therapeutic intervention.