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.
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