Fig. 4: CB2R inhibition in combination with PE ameliorates chronic stress-induced neuroinflammatory changes.

a Chronic stress increases Iba1 granular expression (a1), an effect prevented by AM630 treatment in combination with PE; Iba1 hilar expression remains unchanged in all conditions (a2). b Chronic stress-induced decrease in MBP granular expression is rescued by PE in combination with AM630 treatment (b1); MBP hilar expression remains unaltered when comparing every experimental condition (b2). c GFAP expression in the granular cell layer is unchanged (c1) but uCMS evokes a decrease in GFAP hilar expression, which is reverted by treatment with AM630 in combination with PE. d Representative images of coronal sections of hippocampal DG of all tested conditions, stained for DAPI (blue), Iba1 (green), MBP (red), and GFAP (white) with merged and individual channels; scale bar = 50 µm. The expression of neuroinflammation-related markers e TNFα, f IL1β, g IL10, h arginase, and i iNOS is differentially affected by uCMS and PE in combination with AM630 treatment. Data presented as mean ± SEM and circles represent individual data points (animals) [Student’s t test: **p < 0.01 vs CTRL; Two-way ANOVA: ^#p < 0.05 vs uCMS; further statistical details in Table S4]. uCMS unpredictable chronic mild stress, AM630 CB2R inverse agonist, PE physical exercise.