Fig. 1: Altered PNNs in SUD and MDD.
From: Extracellular matrix abnormalities in the hippocampus of subjects with substance use disorder
A, B Representative low-magnification photomicrographs of CA1 SO PNNs labeled by WFA, scalebars = 0.5 mm. C, D High-magnification photomicrographs of WFA-labeled CA1 SO PNNs, scalebars = 50 µm. E Diagnostic group comparisons of PNN densities in CA1 stratum oriens. Subjects with SUD had significantly increased densities of PNNs (p < 0.007; adjusted for significant effects of cocaine history and PMI) whereas subjects with MDD displayed significantly reduced PNN densities (p < 0.05; adjusted for significant effects of sex and calcium channel blockers). No significant effects were found in the comorbid SUD and MDD group. F Diagnostic group comparisons of normalized hippocampal Pvb gene expression, with a gradient increase between SUD (p < 0.007; adjusted for significant effects of cocaine in the toxicology report), SUD/MDD (p < 0.008; adjusted for significant effects of MDD duration), and MDD (p < 0.005). G Representative PNN quantification overlays of hippocampi from subjects within diagnostic groups. H, I Representative low-magnification photomicrographs of CA4 WFA-labeled glia, scalebars = 0.5 mm. J, K Representative high-magnification WFA-labeled glia, scalebars = 80 50 µm. L Numerical density measurements of CA4 WFA-labeled glial cells in subjects with SUD, MDD, and SUD/MDD. M Normalized gene expression of Gfap was significantly decreased in subjects with comorbid SUD and MDD (p < 0.02; adjusted for significant effects of antidepressant history), but unaffected in either isolated disorder. N Representative WFA+ glia quantification overlays of hippocampi from subjects within diagnostic groups. Error bars are mean ± SEM.
