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Spinal administration of RvE1

Figure 3 - Spinal administration of RvE1

Figure 3 Spinal administration of RvE1 reduces heat hyperalgesia and spontaneous pain by blocking TRPV1 and TNF-α signaling in DRG neurons and spinal presynaptic terminals. (a) CFA-induced heat hyperalgesia and formalininduced second-phase pain in wild-type and Tnfrsf1a−/−; Tnfrsf1b−/− mice. (b) TNF-α–induced heat hyperalgesia and formalin-induced second-phase spontaneous pain in wild-type and Trpv1−/− mice. (c) Prevention of TNF-α–induced heat hyperalgesia by RvE1. *P < 0.05 versus wild-type control (a,b) or vehicle (c), n = 4–6 mice. (d) Effects of RvE1 and capsazepine (CZP, 10 μM) on TNF-α–induced increase in sEPSC frequency in spinal cord lamina II neurons. Bottom, quantification of sEPSC frequency and amplitude. (e) Effects of RvE1, PTX (0.5 μg ml−1), and MEK inhibitor PD98059 and U0126 (1 μM) on capsaicin-induced increase in sEPSC frequency in lamina II neurons. Bottom, quantification of sEPSC frequency and amplitude. *P < 0.05 versus baseline; #P < 0.05 versus TNF-α (d) or capsaicin (e); $P < 0.05; n = 5–10 neurons. (f) Spontaneous pain induced by intrathecal capsaicin and its prevention by RvE1. *P < 0.05 versus RvE1, n = 6 mice. (g) ERK phosphorylation in cultured DRG neurons after TNF-α and capsaicin with or without RvE1. Scale bar, 100 μm. Bottom, percentage of pERK-positive neurons in DRG cultures. *P < 0.05, n = 4 cultures from separate mice. (h) Schematic of RvE1-induced inhibition of inflammatory pain (heat hyperalgesia) via presynaptic mechanisms.


Figure courtesy of Nature Medicine.

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This page last updated: February 26, 2014