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Figure 2 | Molecular Pain

Figure 2

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

Figure 2

A PKA inhibitor (KT5720) inhibits synaptic plasticity but not normal synaptic transmission. Monosynaptic EPSCs were evoked at the PB-CeLC and BLA-CeLC synapses in slices from normal (A, C) and arthritic (6 h postinduction; B, D, E) rats. KT5720 (1 μM, 15 min) inhibited synaptic transmission in neurons from arthritic rats 6 h postinduction (D, n = 7; P < 0.05, paired t-test) but not in control neurons from normal rats (C, n = 7). (A, B) Original recordings of EPSCs (average of 8–10 EPSCs) evoked at the two synapses. (C, D) Averaged EPSC amplitudes (mean ± SE) in the presence of KT5720 normalized to predrug (ACSF) control values (set to 100%). (E) Time course of the inhibitory effect of direct intracellular application of KT5720 (1 μM) through the patch pipette. Each symbol shows averaged EPSC amplitudes (mean ± SE; n = 4) at different times after whole-cell configuration was obtained (t = 0). The inhibitory effect was significant (P < 0.001, compared to the first EPSC after patch formation; Dunnett's Multiple Comparison Test). Insets show EPSCs (average of 8–10 trials) evoked at the PB-CeLC synapse at 1 min (predrug) and at 15 min (KT5720) after patch formation. Whole-cell voltage-clamp recordings were made at -60 mV. * P < 0.05, *** P < 0.001.

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