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Figure 1 | Molecular Pain

Figure 1

From: Facilitation of synaptic transmission and pain responses by CGRP in the amygdala of normal rats

Figure 1

CGRP enhances synaptic transmission in the CeLC in slices from normal animals. (A) Monosynaptic EPSCs evoked at the PB-CeLC synapse with increasing stimulus intensities before and during CGRP (100 nM, 12 min). Individual traces are the average of 10 EPSCs. (B) CGRP (100 nM, 10-14 min) increased input-output function of the PB-CeLC synapse significantly (n = 10, P < 0.0001, F1,198 = 67.97, two-way ANOVA). Input-output curves were generated by plotting peak EPSC amplitude (pA) as a function of afferent fiber volley stimulus intensity (μA). (C) Synaptic facilitation by CGRP was blocked by co-administration of a CGRP1 receptor antagonist (CGRP8-37, 1 μM). Individual traces are the average of 8-10 EPSCs. (D) Cumulative concentration-response relationship of CGRP effects on synaptic transmission at the PB-CeLC synapse (n = 15). Peak amplitudes of monosynaptic EPSCs were averaged for each concentration of CGRP and expressed as percent of predrug control (set to 100%). Concentration-response curve was obtained by non-linear regression analysis using the formula y = A+(B-A)/[1+(10C/10X)D], where A is the bottom plateau, B top plateau, C = log(IC50), and D is the slope coefficient (GraphPad Prism software). CGRP8-37 (1 μM, n = 6) blocked the effect of CGRP (100 nM). CeLC neurons were recorded at -60 mV in slices from naïve untreated animals. Symbols and error bars represent mean ± SEM. *, **, *** P < 0.05-0.001 (Bonferroni posttests).

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