Poulami Ghosh: Effects of Schizophrenia-associated alterations of GABAergic inhibition on Gamma-Band Auditory Steady-Responses in a detailed model of the macaque auditory system

BCCN Berlin / Technische Universität Berlin

Abstract

Schizophrenia (ScZ) is one of the major psychotic disorders that is still diagnosed based on the observed behaviour and psychiatric history of the patients, as the mechanisms underlying circuit dysfunctions in schizophrenic patients remain poorly understood. However, recent studies have proposed Auditory Steady-State Response (ASSR) deficits as a potential biomarker for ScZ. Thus, various computational models have been studied in the hopes of relating different molecular, cellular, or genetic changes to this biomarker and, ultimately, the symptoms of the disorder. Though these studies shed light on the microcircuit alterations associated with ScZ, almost all models studied were relatively simple and abstract and therefore did not allow for a realistic simulation of local field potential (LFP), electroencephalogram (EEG) or magnetoencephalogram (MEG) signals. This made it difficult to compare the models to experimental data. In order to subjugate these shortcomings, it might be advantageous to explore a more complex, biophysically, and anatomically detailed model. Incorporating these kinds of models facilitates an enhanced and refined integration of the microcircuit alterations, thereby enabling a deeper understanding of their intricate mechanisms and functional implications. Hence, this thesis aimed at configuring and using such a detailed model of the macaque auditory cortex to understand the effects of ScZ-associated alterations of gamma-aminobutyric acid (GABA)-ergic inhibition on gamma band ASSR, thereby unravelling the microscopic neuronal parameter changes associated with schizophrenia.

 

 

Additional Information

Master Thesis Defense

 

Organized by

Prof. Dr. Klaus Obermayer   & Prof. Dr. Henning Sprekeler   / Lisa Velenosi

Location: TU Berlin, Marchstraße 23, Room 5.060

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