These morphological alterations are consistent with reactive astrocytes, aligning with the RNA-seq findings of elevated MAOB and GFAP expression in PTSD and resembling astrocytic alterations observed in other psychiatric disorders.31 Together, these results indicate astrocytic GABA dysregulation as a key feature of PTSD, driven by increased MAOB- and ABAT-dependent GABA metabolism, leading us to further investigate the cellular sources of GABA within a PTSD mouse model. The gene discussed is MAOB; the disease is psychiatric disorder.