In contrast to a reported decrease in GABRA1 expression in the DLFPC in individuals with suicidal depression85,86, our TWAS pointed to an increased expression in individuals with depression. GABAA receptors provide critical inhibitory control of the firing of glutamatergic excitatory neurons and they are the binding partner of several drugs in mood disorders and potential drug targets for other psychiatric disorders87-89. Antidepressant effects have been associated with pharmacological modulation of both synaptic90 and extra-synaptic GABAA receptors91, and our findings support the further study of pharmacological modulators of these receptors in the treatment of depression.
