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Curr Opin Anaesthesiol. 2008 Oct;21(5):570-9. doi: 10.1097/ACO.0b013e32830edbdf.

Neuron-glia crosstalk gets serious: role in pain hypersensitivity.

Author information

  • 1Department 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.

PMID:
18784481
[PubMed - indexed for MEDLINE]
PMCID:
PMC2735048
Free PMC Article
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