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. 2014 Feb 17;124(3):1173–1186. doi: 10.1172/JCI72230

Figure 9. Endogenous CASP6 is essential for inducing spinal cord synaptic plasticity in spinal cord slices and LTP in spinal cord of anesthetized mice.

Figure 9

(A) Traces of sEPSCs in lamina IIo neurons of spinal cord slices of WT and Casp6–/– mice before and after CFA inflammation (1 day). (B) Frequency of sEPSCs in WT and Casp6–/– mice before and after CFA inflammation and the effects of the CASP6 inhibitor ZVEID. Note the impairment of CFA-induced sEPSC but not the basal sEPSC increases in Casp6–/– mice. Also note the inhibition of sEPSCs after CFA inflammation by ZVEID in WT but not Casp6–/– mice. *P < 0.05, n = 5–6 neurons. (C) Tetanic stimulation (100 Hz, 1 second, 4 trains, 10 second interval) induces LTP of C-fiber–evoked field potentials in the dorsal horn of anesthetized WT mice but not in Casp6–/– mice. *P < 0.05 (2-way ANOVA, n = 5 mice). (D) Reversal of LTP of C-fiber–evoked field potentials in the dorsal horn of anesthetized mice by the CASP6 inhibitor (10 μg, i.t.), administered 2 hours after LTP induction. *P < 0.05 (2-way ANOVA, n = 5 mice). (E) Traces of sEPSCs before and after capsaicin (CAP) treatment (0.5 μM) and the effects of ZVEID (10 μg/ml). (F) Frequency and amplitude of sEPSCs recorded in E. *P < 0.05, n = 5–6 neurons. (G) Traces of eEPSCs following dorsal root stimulation and the effects of the CASP6 inhibitor in WT and Casp6–/– mice. (H) Amplitude of eEPSCs. Note that the CASP6 inhibitor loses its effects in Casp6–/– mice. *P < 0.05, n = 5–15 neurons.