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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Pain. 2015 May;156(5):825–836. doi: 10.1097/j.pain.0000000000000120

Figure 7. Tempol inhibits excitatory synaptic transmission in CeA neurons in a visceral pain model.

Figure 7

Whole-cell voltage-clamp recordings of monosynaptic EPSCs evoked in CeA neurons by stimulation of presumed afferents from the parabrachial area (see Methods and Discussion) were measured in slices from sham controls and from rats with intracolonic zymosan (“colitis”; 5 h postinjection). A, Input-output functions of EPSCs were significantly increased in slices from zymosan-treated rats (n = 13 neurons) compared to controls (n = 10 neurons; F1,210 = 19.95, P < 0.001, main effect of drug, two-way ANOVA. B, Individual traces show that EPSCs were monosynaptic with constant latency and kinetics. EPSCs were blocked by a non-NMDA receptor antagonist (NBQX, 10 μM). C, Tempol (1 mM) had no effect on baseline transmission in slices from sham controls (n = 5 neurons). D, Tempol inhibited EPSCs in slices from zymosan-treated rats (n = 9 neurons; P < 0.001, Bonferroni posttest). Effects were reversible upon washout (20 min). C,D, Bar histograms show means ± SEM. *** P < 0.001, compared to predrug; # P < 0.05, compared to drug, Bonferroni posttests. E, Time course of the effects of tempol in slices from controls (n = 5 neurons) and from rats with colitis (n = 5). Symbols show means ± SEM. *,**,*** P < 0.05, 0.01, 0.001, colitis compared to control, Bonferroni posttests.