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. 2021 Mar 19;19(3):e3001154. doi: 10.1371/journal.pbio.3001154

Fig 7. Inhibition of IL-1β alleviates microglial ReaChR-induced pain hypersensitivity.

Fig 7

(A) Timeline of experimental procedures for IL-1ra administration and light stimulation during in vivo recordings. (B) The time course of C-fiber–evoked field potentials before and after optogenetic stimulation of spinal microglia in each group (ReaChR+vehicle, ReaChR+IL-1ra, and control+IL-1ra). Vehicle and IL-1ra (10 μL, 50 ng/mL) was topically administered after 30-min baseline recording and subsequently light stimulation was applied at 60 min. Black arrows and red bar indicate the time points of IL-1ra treatment and light stimulation, respectively (A, B). n = 4–5 mice/group. ****P < 0.0001 vehicle vs. IL-1ra. Two-way ANOVA with multi-comparisons. (C, D) Light-induced mechanical (C) and thermal (D) pain hypersensitivity in ipsilateral or contralateral side of ReaChR mice after treatment of IL-1ra or vehicle. Data represented as mean ± SEM, n = 5–8 mice/group. ****P < 0.0001 vehicle vs. IL-1ra. Two-way ANOVA with multi-comparisons. For data plotted in graphs, see S1 Data. (E) A schematic diagram illustrates that optogenetic stimulation of spinal microglia triggers chronic pain in ReaChR mice and highlights the possible mechanism involved. Red light stimulation (1) on the spinal dorsal horn induces microglial activation (2), which releases IL-1β (3) and increases neuronal hyperactivity (4), leading to chronic pain hypersensitivity (5). IL, interleukin; IL-1ra, IL-1 receptor antagonist; ReaChR, red-activated channelrhodopsin.