Additional file 1 of The activation of mGluR4 rescues parallel fiber synaptic transmission and LTP, motor learning and social behavior in a mouse model of Fragile X Syndrome

Additional file 1. Fig. S1. Absence of isoproterenol-induced potentiation of glutamate release in Fmr1KO cerebellar synaptosomes, despite normal β-AR expression and cAMP generation. (A, B) Mean traces from WT (A) and Fmr1 KO (B) cerebellar synaptosomes showing spontaneous release of glutamate in the presence of the Na+ channel blocker tetrodotoxin (1 μM, TTx), and in the presence or absence (control) of isoproterenol (100 μM). (C) Diagram summarizing the isoproterenol effect on glutamate release in the aforementioned conditions from WT (n=8/3 synaptosomal preparations: ***P0.05). Basal release from Fmr1 KO vs WT synaptosomes (#P0.05). (F, G) Quantification of β-AR expressing cerebellar synaptosomes. Immunofluorescence of WT (F) and Fmr1 KO (G) synaptosomes stained with antibodies against β1-AR and the vesicular marker synaptophysin. (H) Co-expression of β-AR/synaptophysin in WT (24.9 ±1.1%, n=16,804/63 fields/2 preparations) and in Fmr1 KO synaptosomes (26.7 ±0.9%, n=18,712/75 fields/2 preparations, P>0.05). Scale bar in F and G, 5 μm. (I) The effect of isoproterenol on the cAMP levels in WT (n=14/3 preparations) is similar (P>0.05) to that in Fmr1 KO synaptosomes (n=15/3 preparations). Bar graphs show raw data and the mean. Two-way ANOVA followed by Tukey test in C. Unpaired student´s t test in (E, H, I).