Fig. 1

Central delivery of laquinimod attenuates motor disability in the acute phase of the disease without affecting cerebellar inflammation. a Clinical score of EAE mice treated by icv injection of laquinimod (1.25 mg/kg/day for 4 weeks) was attenuated at the peak of the acute phase in comparison with EAE-vhl (Mann–Whitney test *p < 0.05). b–f Quantification of several inflammatory markers performed by qPCR in the EAE cerebellum. Bar graphs show that mRNA coding for IBA-1 (b) and M1-like markers (c) were not modified by laquinimod treatment, while there was an increase of M2-like markers Retnla (Ym1) and Tgfb (d). CD3 (e) and GFAP (f) mRNA were unchanged between EAE and EAE-laquinimod mice while Slc1a3 mRNA coding for GLAST (g) was increased in EAE-laquinimod mice (unpaired T test *p < 0.05). All data are represented as mean ± SEM. qPCR results are expressed as fold change of EAE-vhl samples