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Figure 4 | Molecular Pain

Figure 4

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

Figure 4

Selective loss of Runx1-dependent genes in prospective Runx1-transient nociceptors in Tau-Runx1F;Nav1.8Cre mice. (A-C) In situ hybridization (ISH) using the indicated probes on sections through adult lumbar (L4/L5) DRG of Tau-Runx1F control and Tau-Runx1F ;Nav1.8Cre mutant mice. For TrkA (C), both ISH (top pannels) and immunohistochemistry (IHC) (bottom panels) data are shown. Arrows indicate neurons expressing TRPV1high and arrowheads indicate those with TRPV1low. (D, 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 (gray bar) mice. The numbers of Mrgprd+, TRPM8+ and TRPV1high neurons per set of sections (D) were not significantly changed in mutant versus control animals (249 ± 18 versus 243 ± 8 for Mrgprd+ neurons; 99 ± 6 versus 120 ± 9 for TRPM8+ neurons; and 25 ± 2 versus 29 ± 1 for TRPV1high neurons) (p > 0.05). However, CGRP+ and TRPV1low neurons in the mutants (E) decreased from 533 ± 19 to 120 ± 6 (***p < 0.001) and from 231 ± 18 to 82 ± 12 (***p < 0.001), respectively.

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