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Fig. 2 | Molecular Brain

Fig. 2

From: Spinal microglia contribute to sustained inflammatory pain via amplifying neuronal activity

Fig. 2

Depletion of peripheral macrophage reduces formalin induced phase-I acute inflammatory pain. a F4/80-positive cells were largely depleted in hind paw skin 2 days after clodronate liposome treatment (15 ml/kg, i.p.), while Iba1-positive cells in spinal cord DH and DRG were preserved. Representative images of Iba1-positive cells in DH and DRG and F4/80-positive macrophages in hind paw skin from the control and clodronate depletion mice. Scale bars represent 400 μm, 200 μm and 300 μm. b Quantitative data showing the density of Iba1-positive cells in DH, DRG (n.s., no significance, unpaired 2-tailed Student’s t test, n = 6–7 mice/group) and F4/80-positive cells in hind paw skin (***p < 0.001, unpaired 2-tailed Student’s t test, n = 5–6 mice/group) from control and clodronate (Clod.) depletion mice. Data are presented as mean ± SEM. c Basal pain threshold for heat sensitivity (Thermal Withdrawal Latency with Hargreaves Method) and mechanical sensitivity (Mechanical Withdrawal Threshold with von Frey tests) in control and clodronate depletion mice. n = 6 mice/group. Data are presented as mean ± SEM. d Time course (0–60 min) of formalin-induced spontaneous pain behavior (licking/flinching) in control and clodronate depletion mice, as measured every 5 min. Histogram representing formalin-induced Phase-I (1–10 min) and Phase-II (10–60 min) inflammatory pain responses in control and clodronate depletion mice. Note formalin-induced Phase-I acute inflammatory pain is reduced in clodronate depletion mice, while formalin-induced Phase-II inflammatory pain was not significantly affected. Data are presented as mean ± SEM, **P < 0.01, ***P < 0.001, compared to control mice; unpaired 2-tailed Student’s t test, n = 5–8 mice/group

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