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. 2016 Nov 22;27(12):5635–5651. doi: 10.1093/cercor/bhw333

Figure 4.

Figure 4.

Enhanced LTP and abolished LTD in CaMK-Scrib−/− synapses. (A) Enhanced LTP induced by HFS consisting of 2 trains at 100 Hz at CA3-CA1 CaMK-Scrib−/− synapses (red; n = 6/5) compared to Control synapses (black; n = 5, P = 0.01). Scale bars = 5 (Control) and 4 (CaMK-Scrib−/−) ms; 0.1 mV. Data were compared using Mann–Whitney, P = 0.01. (B) Abolished LTD in CA3-CA1 CaMK-Scrib−/− synapses (n = 6/5) that generated LTP following LFS at 1 Hz stimulation in contrast to Control synapses (n = 7/6) that induced LTD. Scale bars = 5 (Control) and 4 (CaMK-Scrib−/−) ms; 0.1 mV. Data were compared using Wilcoxon matched-pairs, P < 0.05 (Control) and P = 0.01 (CaMK-Scrib−/−). (C) A weaker stimulation protocol at 0.5 Hz did not induce any change in Control (n = 5, P = 0.31) or CaMK-Scrib−/− mice (n = 4, P = 0.13). Scale bars = 10 ms; 0.1 mV. Data were compared using Wilcoxon matched-pairs. (D) Long-term depotentiation at CA3-CA1 synapses, potentiated with HFS consisting of 3 trains at 100 Hz followed by LFS at 1 Hz delivery, was impaired in CaMK-Scrib−/− (n = 5) compared to Control mice (n = 6). Scale bars = 10 (Control) and 8 (CaMK-Scrib−/−) ms; 0.1 mV. Data were compared using Wilcoxon matched-pairs, P < 0.05 (Control).