Abstract
Altered GABA/somatostatin (SST) signaling is frequently reported in psychiatric diseases and chronic stress models, participating in symptom emergence. SST+ interneurons from cortical layers and the hippocampus inhibit the dendrites of excitatory neurons, largely through α5-containing GABAA receptors (α5-GABAA-R). Recently, we showed that targeting α5-GABAA-R alleviates symptoms and exerts neurotrophic effects in old mice. Here, we propose to investigate the behavioral and neurotrophic effects of the same compound, combined with its enantiomer, in an animal model of chronic stress.
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.
