Fig. 2

Clemastine short treatment affects the spinal cord pathology in SOD1-G93A mice at symptomatic phase of the disease. a Schematic representation of experimental design. b Spinal cord sections (L3–L5) from WT (~120 days) and vehicle- or clemastine-treated SOD1-G93A mice at PND 120 (n = 4/group) are stained with cresyl violet (scale bar 100 μm) and assessment of motoneuron number is performed by percentage quantification (n = 4/group) (t test referred to WT *p < 0.05 or to vehicle-SOD1-G93A, # p < 0.05). c Spinal cord sections of vehicle- or clemastine-treated SOD1-G93A mice at PND 120 were then stained with anti-NeuN (scale bar = 40 μm). d Equal amounts of total lumbar spinal cord lysates from WT mice (~120 days) and vehicle- or clemastine-treated SOD1-G93A mice at PND 120 (n = 3/group) are subjected to western blotting with anti-Iba1, anti-CD68, anti-ARG-1, anti-CD163 and anti-GAPDH for protein normalisation. Data represent mean ± S.E.M. Statistical significance is calculated by student’s t test referred to WT, * p < 0.05, or to vehicle SOD1-G93A mice, #p < 0.05. e Equal amounts of lumbar spinal cord lysates from vehicle- or clemastine-treated SOD1-G93A mice at PND 120 (n = 3/group) are subjected to western blotting with anti-P2X7, anti-P2X4, anti-P2Y12 and anti-GAPDH. Data represent mean ± S.E.M. Statistical significance was calculated by student’s t test, as referred to vehicle-treated SOD1-G93A mice, * p < 0.05