Figure 1.

Synaptic transmission in SG neurons is enhanced in the arthritis pain model. A,B, Whole-cell voltage-clamp recordings of monosynaptic EPSCs evoked with increasing stimulus intensities in an SG neuron in a spinal cord slice from a normal animal and in an SG neuron in a slice from an arthritic animal (obtained 6 h post-induction of arthritis). Evoked monosynaptic EPSCs had larger amplitudes in arthritis than under control conditions. Square wave electrical stimuli of 150 μs duration were delivered at a frequency < 0.25 Hz. Stimulus intensity was increased from 0–800 μA. Each trace is the average of 3–4 EPSCs. Neurons were held at -60 mV. C, Input-output relationships of monosynaptic EPSC peak amplitudes (pA) evoked in SG neurons from normal rats (n = 16) and from arthritic rats (n = 9) were significantly different. * P < 0.05, ** P < 0.01 (two-way ANOVA followed by Bonferroni posttests). Data are given as the means ± SEM.

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