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. Author manuscript; available in PMC: 2022 Jan 22.
Published in final edited form as: Cell Rep. 2021 Nov 9;37(6):109970. doi: 10.1016/j.celrep.2021.109970

Figure 2. Decreased inhibition in CA1 pyramidal neurons in Cntnap2 KO mice.

Figure 2.

(A) Representative traces of IPSCs recorded from CA1 pyramidal neurons in WT and Cntnap2 KO mice, voltage-clamped at 0 mV, with normalized unitary events (left) demonstrating no differences in the kinetics of IPSCs.

(B) Cumulative distribution and average of IPSC amplitude recorded from pyramidal neurons (WT: 24.24 ± 1.51 pA, n = 41, 7 mice; Cntnap2 KO: 16.22 ± 1.09 pA, n = 38, 8 mice; two-tailed unpaired t test, t (4.22), p < 0.0001; cumulative distribution, Kolmogorov-Smirnof [K-S] test: WT versus KO p < 0.0001).

(C) Cumulative distribution and average plots of IPSC frequency recorded from pyramidal neurons (WT: 6.13 ± 0.41 Hz, n = 41, 7 mice; Cntnap2 KO: 4.54 ± 0.29 Hz, n = 38, 8 mice; two-tailed unpaired t test, t (3.08), p = 0.0029; cumulative distribution, K-S test: WT versus KO p < 0.0001). Note a decreased IPSC amplitude and frequency in pyramidal neurons in Cntnap2 KO mice.

(D–H) Whole-cell patch-clamp IPSC recording from PV+ interneurons located in CA1 pyramidal cell layer in WT and Cntnap2 KO mice.

(D) Representative traces of IPSCs voltage-clamped at 0 mV, with corresponding normalized unitary events in WT and Cntnap2 KO mice.

(E) IPSC amplitude (WT: 28.02 ± 3.33 pA, n = 9, 7 mice; Cntnap2 KO: 23.07 ± 2.70 pA, n = 10, 6 mice; two-tailed unpaired t test, t (1.16), p = 0.2612; cumulative distribution, K-S test: WT versus KO p < 0.0001).

(F) IPSC decay time constant (WT: 1.41 ± 0.12 ms, n = 9, 7 mice; Cntnap2 KO: 2.249 ± 0.32 ms, n = 10, 6 mice; two-tailed unpaired t test, t (2.310), p = 0.0337; cumulative distribution, K-S test: WT versus KO p < 0.0001).

(G) IPSC rise time 10–90 (WT: 2.16 ± 0.26 ms, n = 9, 7 mice; Cntnap2 KO: 3.36 ± 0.52 ms, n = 10, 6 mice; two-tailed unpaired t test, t (1.982), p = 0.0638; cumulative distribution, K-S test: WT versus KO p < 0.0001).

(H) IPSC frequency (WT: 5.06 ± 0.83 Hz, n = 9, 7 mice; Cntnap2 KO: 4.02 ± 0.90 Hz, n = 10, 6 mice; two-tailed unpaired t test, t (0.84), p = 0.41; cumulative distribution, K-S test: WT versus KO p < 0.0001).

(I–O) Whole-cell patch-clamp EPSC recording from PV+ interneurons located in CA1 pyramidal cell layer in WT and Cntnap2 KO mice.

(I) Representative traces of EPSCs voltage-clamped at ‒65 mV, with corresponding normalized unitary events in WT and Cntnap2 KO mice.

(L) EPSC amplitude (WT: 51.76 ± 4.73 pA, n = 11, 7 mice; Cntnap2 KO: 44.87 ± 4.13 pA, n = 12, 6 mice; two-tailed unpaired t test, t (1.102), p = 0.2831; cumulative distribution, K-S test: WT versus KO p < 0.0001).

(M) EPSC decay time constant (WT: 1.73 ± 0.25 ms, n = 11, 7 mice; Cntnap2 KO: 1.43 ± 0.099 ms, n = 12, 6 mice; two-tailed unpaired t test, t (1.123), p = 0.2742; cumulative distribution, K-S test: WT versus KO p < 0.0001).

(N) EPSC rise time 10–90 (WT: 1.33 ± 0.23 ms, n = 11, 7 mice; Cntnap2 KO: 1.79 ± 0.16 ms, n = 12, 6 mice; two-tailed unpaired t test, t (1.639), p = 0.1162; cumulative distribution, K-S test: WT versus KO p < 0.0001).

(O) EPSC frequency (WT: 6.38 ± 1.50 Hz, n = 11, 7 mice; Cntnap2 KO: 5.55 ± 1.17 Hz, n = 12, 6 mice; two-tailed unpaired t test, t (0.44), p = 0.66; cumulative distribution, K-S test: WT versus KO p = 0.87). Results are expressed as mean ± SEM. IPSCs, inhibitory postsynaptic currents; EPSCs, excitatory postsynaptic currents. Data are presented as mean ± SEM.