Figure 5.

EP2 receptor activation enhances glutamate release at sensory synapses onto adult spino-parabrachial neurons. A, Representative plot of current versus time illustrating an increase in the amplitude of primary afferent-evoked EPSCs in response to the bath application of the EP2 receptor agonist butaprost (10 μm). B, Butaprost (5–10 μm) significantly increased monosynaptic primary afferent-evoked EPSC amplitude in projection neurons (n = 13; ***p = 0.0005; Wilcoxon signed-rank test). C, Examples of afferent-evoked EPSCs evoked by paired stimulation in the absence (black) and presence (gray) of butaprost. D, The PPR was significantly decreased by EP2 receptor activation (n = 13; p < 0.0001; repeated-measures 2-way ANOVA; *p < 0.05; **p < 0.01; Bonferroni post-test), indicative of an elevated probability of glutamate release at primary afferent synapses onto mature projection neurons. E, Representative traces illustrating monosynaptic, primary afferent-evoked EPSCs at baseline, during the application of the EP2 receptor agonist butaprost, and 20 min after washout with aCSF. F, Plot of EPSC amplitude versus time demonstrating that the increase in synaptic efficacy evoked by EP2 receptor activation outlasts the presence of the agonist (gray bar). G, Examples of afferent-evoked EPSCs before (Control) and after bath application of the EP3 receptor agonist sulprostone. H, Sulprostone significantly decreased the amplitude of primary afferent-evoked EPSCs in lamina I projection neurons (n = 5; t = 4.177; *p = 0.014; paired t test).