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Trends Neurosci. 2018 Feb;41(2):100-114. doi: 10.1016/j.tins.2017.11.006.

Translational Control Mechanisms in Persistent Pain.

Author information

1
Department of Anesthesia and Alan Edwards Centre for Research on Pain, McGill University, Montréal, QC, H3A 0G1, Canada. Electronic address: arkady.khoutorsky@mcgill.ca.
2
School of Behavioral and Brain Sciences, University of Texas at Dallas, Richardson, TX 75080, USA. Electronic address: Theodore.price@utdallas.edu.

Abstract

Persistent pain, which is poorly treated and estimated to afflict one third of the world's population, is largely mediated by the sensitization of nociceptive neurons. This sensitization involves de novo gene expression to support biochemical and structural changes required to maintain amplified pain signaling that frequently persists even after injury to tissue resolves. While transcription-dependent changes in gene expression are important, recent work demonstrates that activity-dependent regulation of mRNA translation is key to controlling the cellular proteome and the development and maintenance of persistent pain. In this review, we highlight recent advances in translational regulation of gene expression in nociceptive circuits, with a focus on key signaling pathways and mRNA targets that may be tractable for the creation of next-generation pain therapeutics.

KEYWORDS:

local protein synthesis; mRNA translation; pain; sensitization

PMID:
29249459
PMCID:
PMC6004100
DOI:
10.1016/j.tins.2017.11.006
[Indexed for MEDLINE]
Free PMC Article

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