The contribution of gamma bursting to spontaneous gamma activity in schizophrenia

Abstract

Increased spontaneous gamma (30–100 Hz) activity (SGA) has been reported in the auditory cortex in schizophrenia. This phenomenon has been correlated with psychotic symptoms such as auditory hallucinations and could reflect the dysfunction of NMDA receptors on parvalbumin-expressing inhibitory interneurons. Previous findings are from time-averaged spectra, so it is unknown whether increased spontaneous gamma occurs at a constant level, or rather in bursts. To better understand the dynamical nature of spontaneous gamma activity in schizophrenia, here we examined the contribution of gamma bursting and the slope of the EEG spectrum to this phenomenon. The main results from this data set were previously reported. Participants were 24 healthy control participants (HC) and 24 matched participants with schizophrenia (SZ). The data were from EEG recordings during auditory steady-state stimulation, which were localized to bilateral pairs of dipoles in auditory cortex. Time-frequency analysis was performed using Morlet wavelets. Oscillation bursts in the gamma range were defined as periods during which power exceeded 2 standard deviations above the trial-wide average value for at least one cycle. We extracted the burst parameters power, count, and area, as well as non-burst trial power and spectral slope. Gamma burst power and non-burst trial power were greater in SZ than HC, but burst count and area did not differ. Spectral slope was less negative in SZ than HC. Regression modeling found that gamma burst power alone best predicted SGA for both HC and SZ (> = 90% of variance), while spectral slope made a small contribution and non-burst trial power did not influence SGA. Increased SGA in the auditory cortex in schizophrenia is accounted for by increased power within gamma bursts, rather than a tonic increase in gamma-range activity, or a shift in spectral slope. Further research will be necessary to determine if these measures reflect different network mechanisms. We propose that increased gamma burst power is the main component of increased SGA in SZ and could reflect abnormally increased plasticity in cortical circuits due to enhanced plasticity of synapses on parvalbumin-expressing inhibitory interneurons. Thus, increased gamma burst power may be involved in producing psychotic symptoms and cognitive dysfunction.