Figure 2. A2A receptor modulation is lost in symptomatic SOD1(G93A) mice endplates; (A) representative average time-course of mean EPP amplitude change during CGS 21680 (5 nM) bathing and (B) illustrative mean EPP profile facilitation in 12–14 weeks old control (n = 6) and symptomatic mice (n = 6); (C) dose-response alterations in mean EPP amplitude by CGS 21680 (3 nM: n = 8, WT, n = 10, SOD1G93A; 5 nM: n = 10, WT, n = 7, SOD1G93A; 10 nM: n = 11, WT, n = 7, SOD1G93A) were blocked by SCH 58261 at 50 nM in WT mice (n = 4, WT, n = 4, SOD1G93A); (D) SCH 58261 (50 nM) did not affect evoked activity throughout data acquisition (n = 4, WT, n = 7, SOD1G93A); (E) raw recording of spontaneous release variations from a 12–14 weeks old WT and symptomatic SOD1G93A endplate upon CGS 21680 (5 nM) perfusion; effect of A2A receptor activation by CGS 21680 (5 nM) on (F) MEPP frequency (n = 6, WT, n = 5, SOD1(G93A)) (G) GMEPP frequency (n = 4, WT, n = 4, SOD1(G93A)) and (H) quantal content of EPPs (n = 9, WT, n = 7, SOD1(G93A)); *p<0.05 Unpaired t-test; ∂p<0.05 one-way ANOVA with Tukey’s pos-hoc; #p<0.05 Paired t-test (as compared with control value before drug perfusion); control corresponds to 100% in all cases.
