Fig. 5

Siponimod treatment corrects GABAergic defects in EAE striatum. a The glutamatergic transmission was recorded from MSNs of EAE-vehicle and EAE-siponimod mice. The analysis of the increased kinetic properties (rise time, decay time, and half width) of sEPSCs showed that there were no differences between the two groups (unpaired T test, p > 0.05). a’ The frequencies of the glutamatergic currents, increased in EAE striatum, were not corrected by siponimod (unpaired T test, *p > 0.05). a” Electrophysiological traces representative of glutamatergic currents recorded from MSNs of EAE-vehicle and EAE-siponimod mice. b Siponimod restores normal GABAergic frequencies in the striatum of acute phase EAE mice (unpaired T test,*p < 0.05). b’ Electrophysiological traces representative of GABAergic currents recorded from MSNs of EAE-vehicle and EAE-siponimod mice. c The frequencies of the GABAergic currents, reduced in EAE striatum, were completely rescued after 1 h of siponimod incubation in EAE slices (unpaired T test, **p < 0.01)