Fig. 1
From: Nerve injury inhibits Oprd1 and Cnr1 transcription through REST in primary sensory neurons
(a) Peripheral nerve injury induces chronic neuropathic pain hypersensitivities in wild-type mice. Either spared nerve injury (SNI) or sham surgery (Sham) was performed on the left hind limbs of male wild-type mice. Pain symptoms, in terms of ipsilateral hindpaw withdrawal thresholds (withdrawal latency), were determined in response to a noxious pressure stimulus (mechanical hyperalgesia), noxious radiant heat (thermal hyperalgesia), and von Frey filaments (tactile allodynia) over 27 days (Days post-surgery). N = 6 per group. A Student’s t-test was used. P-values are shown (* <0.05; **<0.01; ***<0.001; ****<0.0001) compared with sham group. Data are presented as mean ± SEM. (b–d) SNI results in increased mRNA and protein levels of the REST gene in the injured DRG of wild-type mice, but it does not cause significant changes in the rotarod assays. (b) mRNA samples from the L3/L4 DRG tissues of mice, characterized in Fig. 1a, were used for RT-qPCR analysis of Rest transcripts. Gapdh was used as an internal control. A Student’s t-test was used to measure the p-value. N = 5 mice per group. Data are presented as mean ± SEM. (c) Western blotting assays from the L3/L4 DRG tissues indicated a corresponding increase in the REST protein. M = Molecular weight ladder. Approximate molecular weights in kilodalton are also shown. (d) Rotarod assays of wild-type mice indicate no significant difference between sham and SNI treatment.
