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Figure 1 | Molecular Pain

Figure 1

From: Characterization of two Runx1-dependent nociceptor differentiation programs necessary for inflammatory versus neuropathic pain

Figure 1

Loss of a subset of Runx1-dependent genes in Runx1F/F;Nav1.8Cre L-CKO mice. (A) Schematic showing the timing of "early" Runx1 knockout (using Wnt1-Cre mice, removing Runx1 before the onset of Runx1 expression), and late Runx1 knockout (using Nav1.8-Cre, removing Runx1 during E16-E17). (B-D) In situ hybridization (ISH) using the indicated probes for Runx1-dependent channels and receptors on transverse sections through adult lumbar (L4/L5) DRG from Runx1F/F control mice and Runx1F/F ;Nav1.8Cre L-CKO mice. For Ret and P2X3, double labeling of mRNA (red) with IB4 (green) is shown. For TRPV1 (D), both ISH (top pannels) and immunohistochemistry (IHC) (bottom panels) data are shown. The average numbers of Ret+ and P2X3+ neurons were decreased by 67%, from 599 ± 35 to 199 ± 10 (p < 0.01), and by 56%, from 630 ± 24 to 276 ± 30 (p < 0.001), respectively. Note that the remaining Ret+ and P2X3+ neurons in mutant mice are IB4-. (E) Graph showing the average (± SEM) of the total number of neurons expressing the indicated probes per set of lumbar DRG sections of control (white bar) and mutant (grey bar) mice. Note that the average number of Mrgprb4+ neurons was not significantly changed: from 35 ± 4 to 29 ± 10 (p > 0.05). The number of TRPV1high neurons (arrows) was reduced by 75%, from 21 ± 3 to 5 ± 1 (p < 0.01), whereas the number of TRPV1low (arrowheads) was unchanged, from 210 ± 22 to 218 ± 10 (p > 0.05).

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