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. 2022 Aug 25;13:5014. doi: 10.1038/s41467-022-32558-9

Fig. 6. Enhanced recruitment of NBM cholinergic neurons in a neuropathic pain model and attenuation of neuropathic allodynia by chemogenetic activation of the NBM.

Fig. 6

a, b Typical examples and quantitative summary of expression of the activity marker Fos in cholinergic neurons (ChAT-expressing) of the NBM in naive mice and mice with chronic constriction nerve injury (CCI) in the presence or absence of a low-intensity (0.16 g) mechanical stimulus at the contralateral hindpaw. Scale bar = 50 µm; n = 4 mice/group; P < 0.05 (*0.0168, #0.0065), two-way ANOVA with Sidak’s multiple comparisons tests. c, d Scheme for chemogenetically activating NBM cholinergic neurons expressing hm3D(Gq) with clozapine N-oxide (CNO; c) and validation of its efficacy in increasing Fos expression in comparison to mice expressing mCherry in cholinergic neurons (control; d). d n = 3 mice/group. e–g Comparison of capsaicin-induced nocifensive responses (e) and the development of CCI-induced mechanical hypersensitivity (f) or thermal hypersensitivity (g) between mice with chemogenetic activation of NBM cholinergic neurons and control (mCherry) mice. P values in inset (f) represent ANOVA-based comparison of the two entire stimulus–response curves. n = 5 sham & 6 hM3D(Gq) mice; *P < 0.05 (0.0121 in e; 0.0178 & 0.0231, CCI day 7; 0.0151 & 0.0165, CCI day 11; 0.0209 CCI day 28 in f; <0.0001, CCI day 4; 0.010, CCI day 14 in g), two-way ANOVA with Sidak’s multiple comparisons test. Data are presented as mean +/− SEM.