Work

Altered corollary discharge signaling in the auditory cortex of a mouse model of schizophrenia predisposition

Year: 2023

Type: article

Abstract: The ability to distinguish sensations that are self-generated from those caused by external events is disrupted in schizophrenia patients. However, the neural circuit abnormalities underlying this sensory impairment and its relationship to the risk factors for the disease is not well understood. To address this, we examined the processing of self-generated sounds in male Df(16)A+/− mice, which model one of the largest genetic risk factors for schizophrenia, the 22q11.2 microdeletion. We find that auditory cortical neurons in Df(16)A+/− mice fail to attenuate their responses to self-generated sounds, recapitulating deficits seen in schizophrenia patients. Notably, the auditory cortex of Df(16)A+/− mice displayed weaker motor-related signals and received fewer inputs from the motor cortex, suggesting an anatomical basis underlying the sensory deficit. These results provide insights into the mechanisms by which a major genetic risk factor for schizophrenia disrupts the top-down processing of sensory information.

Source: Nature Communications

DOI: 10.1038/s41467-023-42964-2

Authors: Brian P. Rummell, Solmaz Bikas, Susanne S. Babl, Joseph A. Gogos, Torfi Sigurdsson

Institutions: Goethe University Frankfurt, Max Planck Society, Ernst Strüngmann Institute for Neuroscience, Mortimer B. Zuckerman Mind Brain Behavior Institute, Columbia University

Language: English

Topic: Schizophrenia research and treatment

Subfield: Psychiatry and Mental health

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: gold

Estimated APC paid: $6,227