Fig. 2: Postsynaptic activity of SST cINs regulates the maturation of transient TC inputs.
a Designer receptors exclusively activated by designer drugs (DREADD)-based chemogenetic tools used to test activity-dependent maturation of TC inputs onto SST cINs. 12 to 24 h following AAV injections in the cortex and in the thalamus at P0, DREADD-Gi or -Gq are chronically activated with Clozapine-N-Oxide (CNO) injection twice a day until P8. Recording and synaptic analysis are performed after maturation during early and later mature windows (P9–11 and P28–32). b AAV-driven Cre-dependent ChR2 expression in TCVB inputs at P10. c Example average EPSCs from Ctrl, chronically inhibited with Gi or -activated with Gq SST cINs. d During the early mature window (P9–11), EPSC peak amplitudes and charges are significantly decreased after Gq expression compared to Control and Gi-expressing SST cINs (Amplitudes: Ctrl: 35.08 ± 4.67 pA, n = 13, N = 3 (includes Ctrl from Fig.1); Gi: 31.22 ± 5.17 pA, n = 10, N = 3; Gq: 12.68 ± 2.021 pA, n = 8, N = 3; Kruskal–Wallis test p = 0.0066; Dunn’s multiple comparison test: Ctrl vs Gq p = 0.0038, Gi vs Gq p = 0.0222; Charges, Ctrl: 1.24 ± 0.21 pC; Gi: 1.68 ± 0.69 pC; Gq: 0.08 ± 0.02; Kruskal–Wallis test p = 0.0002; Dunn’s multiple comparison test: Ctrl vs Gq p = 0.0003; Ctrl vs Gi p = 0.999; Gi vs Gq p = 0.0026). e Staining of TC synaptic contacts (VgluT2) onto L5 SST cINs (Homer1). Scale bar: 10 µm. Quantification showing a decrease of the number of synaptic contacts onto SST cINs expressing Gq compared to SST cINs expressing Gi and to P10 Ctrl cells from Fig.1d (Ctrl: 0.116 ± 0.011, n = 86, N = 2; Gi: 0.123 ± 0.009, n = 105; N = 3; Gq 0.074 ± 0.007 n = 94 N = 3; Kruskal–Wallis test p = 0.000016; Dunn’s multiple comparison tests: Ctrl vs Gq p = 0.0078, Ctrl vs Gi p = 0.4542, Gi vs Gq p = 0.000011). Data were presented as mean ± SEM. The number of biologically independent animal replicates = N and cell replicates = n. Source data are provided as a Source Data file.
