Supplementary Fig. 7: HSV-mediated expression of C450M, an inactive control for caRac1, does not affect silent synapse levels.
From: Silent synapses dictate cocaine memory destabilization and reconsolidation
(a,b) Self-administration training results of rats whose electrophysiology results are presented in Supplementary Fig 7d–h (saline: infusions – d1= 15.40 ± 3.01, d2= 8.60 ± 1.44, d3= 9.60 ± 1.99, d4= 13.00 ± 2.24, d5= 9.00 ± 0.894, inactive – d1= 10.20 ± 1.02, d2= 6.40 ± 1.12, d3= 7.20 ± 0.80, d4= 8.80 ± 2.38, d5= 6.20 ± 1.72, n = 5 animals; cocaine: infusions – d1= 39.50 ± 2.74, d2= 34.75 ± 2.16, d3= 31.58 ± 1.82, d4= 32.50 ± 2.16, d5 = 36.25 ± 2.85, inactive – d1= 36.92 ± 10.46, d2= 13.42 ± 2.92, d3= 10.58 ± 3.26, d4= 6.58 ± 1.75, d5= 8.25 ± 2.15, n = 12 animals). (c) Diagram showing the experimental timeline for self-administration, withdrawal, HSV-mediated expression of C450M, and electrophysiology. (d-f) Example EPSCs (inset) over trials in the minimal stimulation assay of C450M-expressing NAcSh MSNs in saline (d)- and cocaine-trained rats (e), and the effects of CP-AMPAR inhibition (f). (h) Summary showing that C450M expression did not affect the % silent synapses in saline- or cocaine-trained rats, and the low % silent synapses in cocaine-trained rats was restored to high levels by naspm inhibition of CP-AMPARs (saline = 6.64 ± 4.15, n = 5 animals; cocaine = 6.04 ± 2.27, n = 6 animals; cocaine naspm = 36.76 ± 3.48, n = 6 animals, F2,14=29.20, p<0.0001, one-way ANOVA; **p<0.01, Bonferroni posttest). See Supplementary Table 1 for exact p values for all comparisons made during posthoc tests. Data presented as mean±SEM.
