Figure 5
Short-term plasticity of excitatory cortical inputs to FSI is modulated during fast frequencies by postsynaptic PV. (a1) Experimental configuration to evoke EPSC in FSI (striatum, CPu; corpus callosum, cc). (a2) An averaged EPSC and its blockage by NBQX (10 μM) are shown. (b1) Averaged EPSC from a PPR protocol at a 50-ms interval. The gray arrow indicates a decrease of the second EPSC in PV−/− FSI compared with PV+/+. Amplitudes were normalized to the first EPSC. (b2) Pooled data for all PPR protocols. PV+/+: n=10; PV+/−: n=8; PV−/−: n=12. (c1) Averaged EPSC from a 50-Hz train. In the PV−/− FSI, the progressive reduction of EPSC amplitudes is more accentuated than in the PV+/+ FSI. Amplitudes were normalized to the first EPSC. (c2) Pooled data for 50-Hz trains. The second EPSC is significantly reduced in PV−/− and PV+/− FSIs compared with PV+/+. A two-way ANOVA test demonstrated a significant difference between genotypes (PV+/+: n=10; PV+/−: n=8; PV−/−: n=12; P<0.001). (d1) Averaged EPSCs from a 100-Hz train. At higher frequency, a marked reduction of the second EPSC is observed in PV−/− and PV+/− FSIs compared with PV+/+. Amplitudes were normalized to the first EPSC. (d2) Pooled data for 100-Hz trains. The second EPSC is also significantly reduced in PV−/− and PV+/− FSIs compared with PV+/+. The two-way ANOVA test confirmed a significant difference between genotypes (PV+/+: n=10; PV+/−: n=8; PV−/−: n=11; P<0.001). The same color code (black and red) applies for b1–d2. Averages are from 20 tests recorded at 4-s intervals in a FSI (b1, c1 and d1). Dotted line in b2 represents unity. All values are presented as means±s.e.m., bars denoting the s.e.m. *P<0.05, **P<0.01, ***P<0.001 Student’s t-test. ANOVA, analysis of variance; EPSC, excitatory postsynaptic current; FSI, fast-spiking interneuron; ISI, inter-spike interval; NBQX, 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione; PPR, paired-pulse ratio; PV, parvalbumin.
