Abstract
Postmortem studies of schizophrenia have yielded definitive evidence for abnormalities of cortical GABAergic neurons. However, few studies have delineated how the GABA neurons are functionally impaired and how their abnormalities cause symptoms of the illness. Thelin et al. (in this issue) recorded in vivo task-related spike firings of individual neurons in the primary auditory cortex in a mouse model of the 15q13.3 microdeletion syndrome, which is associated with an approximately 10-fold increased risk for developing schizophrenia. This article is protected by copyright. All rights reserved.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
