The paper was published by Fee et al. in the International Journal of Neuropsychopharmacology.
Patients suffering from mood and anxiety disorders often exhibit a deficit in brain inhibition. This deficit in brain inhibition is due do dysfunctional somatostatin (SST) cells, causing mood and cognitive symptoms in patients. Using transgenic mice in which the SST cell function can be silenced, Fee et al demonstrated that silencing the SST cells induced mood and cognitive deficits. Interestingly, the mice were treated with an experimental drug targeting a specific subset of receptors to which to SST cells usually signal through: the α5-GABAA receptors. Targeting these receptors led to antidepressant and anxiolytic-like improvement in the animal phenotype, and partially improved cognitive functions.