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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: VPAC1 receptor (Vipr1)-deficient mice exhibit ameliorated experimental autoimmune encephalomyelitis, with specific deficits in the effector stage

Fig. 1

Reduced clinical EAE and histopathology in VPAC1 KO vs. WT mice. EAE was induced by immunizing mice subcutaneously with 100 μg of MOG35–55 in CFA supplemented with Mycobacterium tuberculosis. EAE clinical scores were monitored daily on a scale of 0 to 4 as described in the “Methods” section. Spinal cord microsections were stained with luxol fast blue (for demyelination) and hematoxylin-eosin (for immune cell infiltration), and histopathology was scored from 0 to 3 as described in the “Methods” section. a Clinical curve displaying mean clinical scores ± SEM of immunized WT vs. VPAC1 KO mice, representing the summation of three experiments (n = 18 mice per genotype). b Clinical curve displaying mean clinical scores ± SEM of immunized WT mice pretreated with PBS or a VPAC1 antagonist, representing the summation of two experiments (n = 15 for WT-PBS and n = 11 for WT-VPAC1 antagonist). c Mean histopathological score at day 30 of three experiments ± SEM (n = 12 in each group). ***p < 0.001 Student’s t test. ND = not determined. d Low- (×4) and e high- (×20) magnification photomicrographs of day 30 WT and VPAC1 KO mice transverse thoracolumbar spinal cord sections

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