Figure 4.

Enhanced synaptic facilitation by CGRP in the arthritis pain model. A, B, Whole-cell voltage-clamp recordings of monosynaptic EPSCs in an SG neuron in a slice from a normal animal (A) and in another SG neuron in a slice from an arthritic animal (B, 6 h postinduction of arthritis). CGRP (10 nM) potentiated synaptic transmission more strongly in arthritis than under normal conditions. Square wave electrical stimuli of 150 μs duration were delivered at a frequency < 0.25 Hz. Each trace is the average of 8–10 EPSCs. C, Concentration-response data show that the maximum effect (efficacy) of CGRP was significantly greater in SG neurons from arthritic rats (n = 16) compared to control neurons from normal animals (n = 10). Peak EPSC amplitudes during each concentration of CGRP were averaged and expressed as percent of predrug (baseline) control (100%). Sigmoid curves were fitted to the data using the following formula for nonlinear regression (GraphPad Prism 3.0; Y = A+(B-A)/[1+(10C/10X)D], where A = bottom plateau, B = top plateau, C = log(EC50), D = slope coefficient. Symbols show mean ± SEM. Neurons were held at -60 mV. CGRP was applied by superfusion of the slice in ACSF for 10 min. * P < 0.05 (two-way ANOVA followed by Bonferroni posttests).

Bird et al. Molecular Pain 2006 2:31   doi:10.1186/1744-8069-2-31
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