Extended Data Fig. 5: Tissue-injury-associated allodynia is relieved by chemogenetic or optical inhibition of POGlu neurons. | Nature Neuroscience

Extended Data Fig. 5: Tissue-injury-associated allodynia is relieved by chemogenetic or optical inhibition of POGlu neurons.

From: Distinct thalamocortical circuits underlie allodynia induced by tissue injury and by depression-like states

Extended Data Fig. 5

a, Schematic of chemogenetic experiments in CaMKII-Cre mice. b, Typical image showing the injection site within the S1HL by AAV-DIO-hM4Di-mCherry. Scale bar, 500 µm. c, Example recording of spontaneous spikes (left) and statistics data (right) showing the S1HLGlu firing rates in CaMKII-Cre mice after injected AAV-DIO-hM4Di-mCherry or AAV-DIO-mCherry (n = 21 cells from 3 mice for mCherry; n = 15 cells from 3 mice for hM4Di-mCherry; t34 = 3.246, P = 0.003). d, Whole-cell recording showing the effect of CNO on AAV-DIO-hM4Di-mCherry or AAV-DIO-mCherry expressing S1HLGlu neurons (n = 3 cells from 3 mice for mCherry; n = 4 cells from 4 mice for hM4Di-mCherry; F1,5 = 19.89, P = 0.007). e, Effects of chemogenetic inhibition of S1HLGlu neurons on pain threshold in CFA 3D (left) or SNI 7D (right) mice (n = 6 mice per group; CFA model: F1,10 = 158.3, P < 0.0001; SNI model: F1,10 = 119.6, P < 0.0001). f, Schematic of chemogenetic in CaMKII-Cre mice. g, Typical images showing the injection site within the PO (left) and PF (right). Scale bars, 200 µm. h, Effects of chemogenetic inhibition of PFGlu neurons on pain threshold in CFA 3D (left) or SNI 7D (right) mice (n = 5 mice per group; CFA model: F1,8 = 1.084, P = 0.328; SNI model: F1,8 = 0.897, P = 0.371). i, Schematic of optogenetics experiments in CaMKII-Cre mice. j, Raster plot (top) and peri-stimulus time histogram (bottom) showing the POGlu firing rates in CaMKII-Cre mice with PO infusion of AAV-DIO-eNpHR-EYFP. k, Sample trace of the action potential recorded from AAV-DIO-eNpHR-EYFP-expressing POGlu neurons via photostimulation (594 nm) in acute slices from CaMKII-Cre mice. l, Schematic of chemogenetic experiments in CaMKII-Cre mice. m, Example recording of spontaneous spikes (left) and statistics data (right) showing the POGlu firing rate in CaMKII-Cre mice after injected AAV-DIO-hM3Dq-mCherry or AAV-DIO-mCherry (n = 31 cells from 3 mice per group; t60 = 3.039, P = 0.004). n, Whole-cell recording showing the effect of CNO on AAV-DIO-hM3Dq-mCherry or AAV-DIO-mCherry expressing POGlu neurons (n = 3 cells from 3 mice for mCherry; n = 4 cells from 4 mice for hM3Dq-mCherry; F1,5 = 10.72, P = 0.022). o, Effects of chemogenetic activation of POGlu neurons on pain threshold in naïve mice (n = 5 mice per group; F1,8 = 105.1, P < 0.0001). Significance was assessed by unpaired Student’s t-test in c and m, two-way repeated measures ANOVA with post hoc comparison between groups in d, e, h, n and o. All data are presented as the mean ± s.e.m. * P < 0.05, ** P < 0.01, *** P < 0.001. For detailed statistics information, see Supplementary Table 1.

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