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

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.

• Authors: Ke Ren, Ronald Dubner
• Journal: Current opinion in anaesthesiology (Curr Opin Anaesthesiol) Vol. 21 Issue 5 Pg. 570-9 (Oct 2008) ISSN: 1473-6500 [Electronic] United States
• PMID: 18784481 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)

Chemical References

• Cytokines

Topics

• Astrocytes (physiology)
• Cell Communication (physiology)
• Cytokines (physiology)
• Humans
• Hyperalgesia (metabolism, physiopathology)
• Neuroglia (metabolism, physiology)
• Neurons (physiology)
• Peripheral Nerve Injuries
• Receptor Cross-Talk
• Signal Transduction