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Figure 1 | Molecular Pain

Figure 1

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

Figure 1

Synaptic plasticity in CeLC neurons in the arthritis pain model. Input-output functions of CeLC neurons were measured in slices from arthritic animals (6 h postinduction) and in slices from normal animals. Monosynaptic excitatory postsynaptic currents (EPSCs) were evoked in CeLC neurons by electrical stimulation of the PB-CeLC (A) and BLA-CeLC (B) synapses with increasing intensities. Input-output curves were generated by plotting peak EPSC amplitude (pA) as a function of afferent fiber volley stimulus intensity (μA). Input-output functions of neurons from arthritic animals (n = 19) were significantly different from those of control neurons (n = 16) at the PB-CeLC (P < 0.0001, F 1,363 = 66.65) and BLA-CeLC (P < 0.0001, F 1,363 = 43.30, two-way ANOVA) synapses. Individual traces (mean of 8–10 trials) show monosynaptic EPSCs recorded in one CeLC neuron from a normal rat and another CeLC neuron from an arthritic rat. Whole-cell voltage-clamp recordings were made at -60 mV. * P < 0.05, ** P < 0.01, *** P < 0.001 (Bonferroni post-tests).

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