Fig. 5: TIAN treatment more directly counteracts SNI-specific gene expression changes in the NAc.
From: Tianeptine promotes lasting antiallodynic effects in a mouse model of neuropathic pain
A Venn diagram comparing TIANvSal_SNI, TIANvSal_Sham, DMIvSal_SNI, and DMIvSal_Sham conditions (n = 4–6 animals/condition). B RRHO plot depicting threshold-free concordance between TIAN and DMI effects on gene expression in SNI animals, despite vast differences in DEGs. C Volcano plot depicting DEGs from the direct TIANvDMI_SNI comparison (blue = p-adj < 0.1, yellow = p-nom < 0.05). D Top canonical pathways predicted by Qiagen IPA from the TIANvDMI_SNI comparison (p-nominal < 0.05). E, F Bar graph depicting upstream regulators predicted to be activated (top) and inhibited (bottom) in SNI animals treated with TIAN compared to DMI (p value of overlap < 0.05). G Venn diagram comparing SNIvSham_Saline DEGs to TIANvSal_SNI and DMIvSal_SNI DEGs. H Union heatmap comparing TIANvSal_SNI and DMIvSal_SNI p-nom < 0.05 gene expression changes to SNIvSham_Sal DEGs, a reference control for nerve injury-induced DEGs, on a log2FC > |0.32| cutoff. I–K GO: Molecular Function (GO: MF; Enrichr) mechanisms associated with shared, TIAN-unique, and DMI-unique counter-regulated, SNI-specific DEGs (p-nom < 0.05), respectively.
