Ke Ren1, Ronald Dubner. 1. Department of Neural and Pain Sciences, Dental School and Program in Neuroscience, University of Maryland, Baltimore, Maryland 21201-1586, USA.
Abstract
PURPOSE OF REVIEW: Recent studies show that peripheral injury activates both neuronal and nonneuronal or glial components of the peripheral and central cellular circuitry. The subsequent neuron-glia interactions contribute to pain hypersensitivity. This review will briefly discuss novel findings that have shed light on the cellular mechanisms of neuron-glia interactions in persistent pain. RECENT FINDINGS: Two fundamental questions related to neuron-glia interactions in pain mechanisms have been addressed: what are the signals that lead to central glial activation after injury and how do glial cells affect central nervous system neuronal activity and promote hyperalgesia? SUMMARY: Evidence indicates that central glial activation depends on nerve inputs from the site of injury and release of chemical mediators. Hematogenous immune cells may migrate to/infiltrate the brain and circulating inflammatory mediators may penetrate the blood-brain barrier to participate in central glial responses to injury. Inflammatory cytokines such as interleukin-1beta released from glia may facilitate pain transmission through its coupling to neuronal glutamate receptors. This bidirectional neuron-glia signaling plays a key role in glial activation, cytokine production and the initiation and maintenance of hyperalgesia. Recognition of the contribution of the mutual neuron-glia interactions to central sensitization and hyperalgesia prompts new treatment for chronic pain.
PURPOSE OF REVIEW: Recent studies show that peripheral injury activates both neuronal and nonneuronal or glial components of the peripheral and central cellular circuitry. The subsequent neuron-glia interactions contribute to painhypersensitivity. This review will briefly discuss novel findings that have shed light on the cellular mechanisms of neuron-glia interactions in persistent pain. RECENT FINDINGS: Two fundamental questions related to neuron-glia interactions in pain mechanisms have been addressed: what are the signals that lead to central glial activation after injury and how do glial cells affect central nervous system neuronal activity and promote hyperalgesia? SUMMARY: Evidence indicates that central glial activation depends on nerve inputs from the site of injury and release of chemical mediators. Hematogenous immune cells may migrate to/infiltrate the brain and circulating inflammatory mediators may penetrate the blood-brain barrier to participate in central glial responses to injury. Inflammatory cytokines such as interleukin-1beta released from glia may facilitate pain transmission through its coupling to neuronal glutamate receptors. This bidirectional neuron-glia signaling plays a key role in glial activation, cytokine production and the initiation and maintenance of hyperalgesia. Recognition of the contribution of the mutual neuron-glia interactions to central sensitization and hyperalgesia prompts new treatment for chronic pain.
Authors: E Milligan; V Zapata; D Schoeniger; M Chacur; P Green; S Poole; D Martin; S F Maier; L R Watkins Journal: Eur J Neurosci Date: 2005-12 Impact factor: 3.386
Authors: Adelina Holguin; Kevin A O'Connor; Joseph Biedenkapp; Jay Campisi; Julie Wieseler-Frank; Erin D Milligan; Michael K Hansen; Leah Spataro; Elena Maksimova; Courtenay Bravmann; David Martin; Monika Fleshner; Steven F Maier; Linda R Watkins Journal: Pain Date: 2004-08 Impact factor: 6.961
Authors: Yue Wu; Erin L Lousberg; Lachlan M Moldenhauer; John D Hayball; Janet K Coller; Kenner C Rice; Linda R Watkins; Andrew A Somogyi; Mark R Hutchinson Journal: Br J Pharmacol Date: 2012-03 Impact factor: 8.739
Authors: Mark R Hutchinson; Yehuda Shavit; Peter M Grace; Kenner C Rice; Steven F Maier; Linda R Watkins Journal: Pharmacol Rev Date: 2011-07-13 Impact factor: 25.468