Cell-type enrichment analysis of the differentially expressed genes indicates that the effective treatments (feno and tesa) target a subset of GABAergic interneurons in the amygdala that beza does not. Results from WGCNA show that GABAergic signaling is regulated in a coordinated manner by feno and tesa in the amygdala. The change in expression of GABA neurons is consistent with long-standing evidence for the GABAergic system in alcohol actions 62. A potential increase in GABAergic signaling resulting from expression changes of multiple GABA-related transcripts could play a role in the anticonvulsant properties of PPAR agonists 43, 45 and the ability of these drugs to suppress alcohol withdrawal signs 59.
