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Neurobiol Pain. 2018 Aug-Dec;4:20-26. doi: 10.1016/j.ynpai.2018.03.003. Epub 2018 Apr 3.

Translation regulation in the spinal dorsal horn - A key mechanism for development of chronic pain.

Author information

1
Department of Anesthesia, McGill University, Montréal, QC H3A 0G1, Canada.
2
Department of Psychology, McGill University, Montréal, QC H3A 1B1, Canada.
3
Alan Edwards Centre for Research on Pain, McGill University, Montréal, QC H3A 0G1, Canada.

Abstract

Chronic pain is a pathological condition characterized by long-lasting pain after damaged tissue has healed. Chronic pain can be caused and maintained by changes in various components of the pain pathway, including sensory neurons, spinal cord and higher brain centers. Exaggerated sensitivity and responsiveness of spinal nociceptive circuits, representing maladaptive plasticity, play key roles in the amplification of peripheral signals in chronic pain conditions. This spinal amplification mechanism profoundly contributes to the development and maintenance of chronic pain hypersensitivity in response to peripheral injury, and in some cases occurs independently of the peripheral stimulus. Long-lasting changes in the activity of spinal neurons are caused by alterations in their cellular proteome, which relies on de novo gene expression. Recent evidence indicates that translational control of gene expression plays a major role in determining protein levels, and is intricately involved in different forms of intrinsic and synaptic plasticity. In this review, we summarize findings supporting a key role for translational control in spinal cord-dependent mechanisms of chronic pain, and present recent approaches to reverse persistent pain by targeting these mechanisms.

Conflict of interest statement

Conflict of interest The authors declare that they have no conflicts of interest.

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