An Approach to Identify Nerve Injury-Evoked Changes that Contribute to the Development or Protect Against the Development of Sustained Neuropathic Pain

Recio-Pinto, Esperanza; Norcini, Monica; Blanck, Thomas J. J.

doi:10.5772/30036

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References 102 publications

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“…However, behavioral discrepancies emerged over time. The Sural-SNI animals maintained strong mechanical allodynia throughout the entire observation period of 85 days (Figure 1A , dark blue line), consistent with previous reports (Decosterd and Woolf, 2000 ; Suter et al, 2003 ); however, the Tibial-SNI animals started to recover from mechanical allodynia at about 2 weeks post-surgery, and displayed almost full recovery by day 40 post-surgery (Figure 1A , dark green line) (Recio-Pinto et al, 2012 ). The naïve and sham operated animals, showed no significant decrease in the threshold for mechanical allodynia (Figure 1A , black and purple lines, respectively).…”

Section: Resultssupporting

confidence: 90%

An approach to identify microRNAs involved in neuropathic pain following a peripheral nerve injury

et al. 2014

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Peripheral nerve injury alters the expression of hundreds of proteins in dorsal root ganglia (DRG). Targeting some of these proteins has led to successful treatments for acute pain, but not for sustained post-operative neuropathic pain. The latter may require targeting multiple proteins. Since a single microRNA (miR) can affect the expression of multiple proteins, here, we describe an approach to identify chronic neuropathic pain-relevant miRs. We used two variants of the spared nerve injury (SNI): Sural-SNI and Tibial-SNI and found distinct pain phenotypes between the two. Both models induced strong mechanical allodynia, but only Sural-SNI rats maintained strong mechanical and cold allodynia, as previously reported. In contrast, we found that Tibial-SNI rats recovered from mechanical allodynia and never developed cold allodynia. Since both models involve nerve injury, we increased the probability of identifying differentially regulated miRs that correlated with the quality and magnitude of neuropathic pain and decreased the probability of detecting miRs that are solely involved in neuronal regeneration. We found seven such miRs in L3-L5 DRG. The expression of these miRs increased in Tibial-SNI. These miRs displayed a lower level of expression in Sural-SNI, with four having levels lower than those in sham animals. Bioinformatic analysis of how these miRs could affect the expression of some ion channels supports the view that, following a peripheral nerve injury, the increase of the seven miRs may contribute to the recovery from neuropathic pain while the decrease of four of them may contribute to the development of chronic neuropathic pain. The approach used resulted in the identification of a small number of potentially neuropathic pain relevant miRs. Additional studies are required to investigate whether manipulating the expression of the identified miRs in primary sensory neurons can prevent or ameliorate chronic neuropathic pain following peripheral nerve injuries.

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Section: Resultssupporting

confidence: 90%