University of Hertfordshire

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Original languageEnglish
JournalBMC Neuroscience
Volume21
DOIs
Publication statusAccepted/In press - 2020
Event29th Annual Computational Neuroscience Meeting: CNS*2020 -
Duration: 18 Jul 2020 → …

Abstract

The mechanisms underlying circuit dysfunctions in schizophrenia (SCZ) remain poorly understood. Auditory steady-state response (ASSRs), especially in the gamma and beta band, have been suggested as a potential biomarker for SCZ. While the reduction of 40Hz power for 40Hz drive has been well established and replicated in SCZ patients, studies are inconclusive when it comes to an increase in 20Hz power during 40Hz drive. There might be several factors explaining the inconsistencies, including differences in the sensitivity of the recording modality (EEG vs MEG), differences in stimuli (click-trains vs amplitude-modulated tones) and also large differences in the amplitude of the stimuli.

Here, we used a computational model of ASSR deficits in SCZ, in which increased IPSC decay times at GABAergic synapses produce ASSR deficits as seen experimentally. We investigated the effect of input strength on gamma and beta band power during gamma ASSR stimulation. We found that the pronounced increase in beta power during gamma stimulation seen experimentally could only be reproduced in the model for a specific range of input strengths. More specifically, if the input was too weak the network failed to produce a strong oscillatory rhythm. When the input was in the specific range, the rhythmic drive at 40Hz produced a strong 40Hz rhythm in the control network, however, in the ‘SCZ-like’ network, the prolonged inhibition led to a so-called ‘beat-skipping’, where the network would only strongly respond to every other input. This mechanism was responsible for the emergence of the pronounced 20Hz beta peak in the power spectrum. However, if the input exceeded a certain strength value, the 20Hz peak in the power spectrum disappeared again. In this case, prolonged inhibition due to the increased IPSC times was insufficient to suppress the now stronger gamma drive from the input, resulting in an absence of the beat-skipping and single peak at 40Hz in the power spectrum.

Here, we employed an established model of gamma and beta band ASSR deficits in SCZ to explore the dependence of a beta component in response to gamma drive on the strength of the input. Our finding that the beta component only existed for a specific range of input strengths might explain the seemingly inconsistent reporting in experimental studies and suggests that future ASSR studies should explicitly explore different amplitudes of their stimuli.

ID: 21693094