Extended Data Fig. 4: Enhanced excitability of GluLHA neurons in CFA 10 d mice are reversed by chemogenetic inhibition of GluACC neurons.
From: A neural circuit for the suppression of feeding under persistent pain
a, Representative confocal images (left) and statistical analysis (right) showing c-Fos-positive neurons in the LHA of saline and CFA 10 d mice injected with AAV-DIO-mCherry or AAV-DIO-hM4Di-mCherry into the ACC (n = 8 slices from 6 mice per group; F2,21 = 81.58, P < 0.0001). Scale bars, 200 µm. b, Representative confocal images (left) and statistical analysis (right) showing that c-Fos-labeled neurons in the LHA of CFA 10 d mice predominantly colocalized with the glutamate antibody (n = 7 slices from 6 mice). Scale bar, 10 µm. c, Sample traces of voltage responses to a stepwise series of hyperpolarizing currents (0 to −50 pA, −10 pA/step; duration: 500 ms) recorded in GluLHA neurons of saline::mCherry (top), CFA::mCherry (upper middle), and CFA::hM4Di-mCherry (lower middle) groups and voltage-current plots derived from these traces (bottom). d,e, RMP (d) and Rin (e) data of the three groups (Saline::mCherry, n = 40 cells from 8 mice; CFA::mCherry, n = 47 cells from 8 mice; CFA::hM4Di-mCherry, n = 47 cells from 8 mice; d, F2,21 = 12.57, P < 0.001). Significance was assessed by one-way ANOVA with post hoc comparison between groups in (a), and nested one-way ANOVA with post hoc comparison between groups in (d and e). All data are presented as the mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001.
