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Figure 5 | Molecular Pain

Figure 5

From: PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior

Figure 5

Additive effect of PKA and ERK inhibitors on NMDA receptor-mediated synaptic plasticity. (A, B) KT5720 (KT, 1 μM, 15 min; n = 3) inhibited the pharmacologically (with NBQX, 20 μM; bicuculline, 30 μM) isolated NMDA receptor-mediated synaptic component in slices from arthritic rats (P < 0.001, repeated-measures ANOVA with Bonferroni post-tests). Co-application of KT5720 and U0126 (1 μM, n = 3) further decreased the synaptic response (P < 0.001, Bonferroni post-tests). (C, D) U0126 (1 μM, 15 min) applied alone (n = 3) or together with KT5720 (n = 3) inhibited the NMDA component in the arthritis pain model (P < 0.05–0.001, Bonferroni post-tests). (E) Coapplication of KT5720 and U0126 (n = 6) had a significantly greater effect than each compound alone (P < 0.05–0.01, one-way ANOVA with Bonferroni post-tests). A negative structural analogue of U0126 (U0124, 1 μM, n = 3) had no effect. Bar histograms show averaged EPSC amplitudes (mean ± SE) normalized to predrug control values (set to 100%). (A, C) Monosynaptic EPSCs (average of 8–10 traces) recorded at -60 mV and +20 mV. (B, D) Time course of drug effects at -60 mV and +20 mV. Each symbol shows averaged EPSC amplitudes (mean ± SE) normalized to predrug control (set to 100%). * P < 0.05, ** P < 0.01, *** P < 0.001 (compared to predrug values); + P < 0.05, ++ P < 0.01 (compared to each drug alone).

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