Figure 3.

CGRP8-37 inhibits pain-related synaptic plasticity but has no significant effect on normal synaptic transmission. A, B, CGRP8-37 (1 μM) inhibited monosynaptic EPSCs recorded in an SG neuron in a slice from an arthritic rat (B) but not in another SG neuron in a slice from a normal rat (A). Each trace is the average of 8–10 monosynaptic EPSCs. C, D, CGRP8-37 (1 μM) significantly inhibited the EPSC peak amplitude (C), a measure of synaptic strength, and area under the curve (total charge, D) in SG neurons in slices from arthritic rats (P < 0.01, paired t-test, n = 5) but not in control neurons (n = 7) from normal rats. Analysis of raw data (pA, pC) is shown on the left; normalized data (% of predrug values) are shown on the right in C and D. Voltage-clamp recordings were made at -60 mV. CGRP8-37 was applied by superfusion of the slice in ACSF for 10–12 min. ** P < 0.01 (paired t-test).

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