Page 287 - MEGIN Book Of Abstracts - 2023

The beta component of gamma-band auditory the beta component only existed for a specific range of
steady-state responses in patients with input strengths might explain the seemingly inconsis-
schizophrenia (2021) tent reporting in experimental studies and suggests
that future ASSR studies should systematically explore
Metzner, Christoph; Steuber, Volker different amplitudes of their stimuli. Furthermore,
we provide a mechanistic link between a microcircuit
School of Physics, Engineering and Computer Science, Uni- alteration and an electrophysiological marker in schizo-
versity of Hertfordshire, Hatfield, UK. cmetzner@ni.tu-berlin.de phrenia and argue that more complex ASSR stimuli are
needed to disentangle the nonlinear interactions of
ABSTRACT The mechanisms underlying circuit dys- microcircuit alterations. The computational modelling
functions in schizophrenia (SCZ) remain poorly un- approach put forward here is ideally suited to facilitate
derstood. Auditory steady-state responses (ASSRs), the development of such stimuli in a theory-based
especially in the gamma and beta band, have been fashion.
suggested as a potential biomarker for SCZ. While the
reduction of 40 Hz power for 40 Hz drive has been well Scientific reports (2021), Vol. 11, No. 1 (34650135) (0
established and replicated in SCZ patients, studies are citations)
inconclusive when it comes to an increase in 20 Hz
power during 40 Hz drive. There might be several fac-
tors explaining the inconsistencies, including differenc- Current findings and perspectives on aberrant
es in the sensitivity of the recording modality (EEG vs neural oscillations in schizophrenia (2021)
MEG), differences in stimuli (click-trains vs amplitude-
modulated tones) and large differences in the ampli- Hirano, Yoji; Uhlhaas, Peter J
tude of the stimuli. Here, we used a computational
model of ASSR deficits in SCZ and explored the effect of Institute of Industrial Science, The University of Tokyo, Tokyo,
three SCZ-associated microcircuit alterations: reduced Japan; Institute of Neuroscience and Psychology, University of
GABA activity, increased GABA decay times and NMDA Glasgow, Glasgow, UK
receptor hypofunction. We investigated the effect of
input strength on gamma (40 Hz) and beta (20 Hz) ABSTRACT There is now consistent evidence that
band power during gamma ASSR stimulation and saw neural oscillation at low- and high-frequencies consti-
that the pronounced increase in beta power during tute an important aspect of the pathophysiology of
gamma stimulation seen experimentally could only schizophrenia. Specifically, impaired rhythmic activity
be reproduced in the model when GABA decay times may underlie the deficit to generate coherent cognition
were increased and only for a specific range of input and behavior, leading to the characteristic symptoms
strengths. More specifically, when the input was in this of psychosis and cognitive deficits. Importantly, the
specific range, the rhythmic drive at 40 Hz produced a generating mechanisms of neural oscillations are rela-
strong 40 Hz rhythm in the control network; however, tively well-understood and thus enable the targeted
in the 'SCZ-like' network, the prolonged inhibition search for the underlying circuit impairments and novel
led to a so-called 'beat-skipping', where the network treatment targets. In the following review, we will sum-
would only strongly respond to every other input. This marize and assess the evidence for aberrant rhythmic
mechanism was responsible for the emergence of the activity in schizophrenia through evaluating studies
pronounced 20 Hz beta peak in the power spectrum. that have utilized Electro/Magnetoencephalography to
The other two microcircuit alterations were not able to examine neural oscillations during sensory and cogni-
produce a substantial 20 Hz component but they fur- tive tasks as well as during resting-state measurements.
ther narrowed the input strength range for which the These data will be linked to current evidence from post-
network produced a beta component when combined mortem, neuroimaging, genetics, and animal models
with increased GABAergic decay times. Our finding that that have implicated deficits in GABAergic interneurons

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