Neuron–glia crosstalk gets serious: role in pain hypersensitivity
- 1 October 2008
- journal article
- review article
- Published by Ovid Technologies (Wolters Kluwer Health) in Current Opinion In Anesthesiology
- Vol. 21 (5), 570-579
- https://doi.org/10.1097/aco.0b013e32830edbdf
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.Keywords
This publication has 116 references indexed in Scilit:
- IL-1ra alleviates inflammatory hyperalgesia through preventing phosphorylation of NMDA receptor NR-1 subunit in ratsPain, 2008
- Distinct roles of matrix metalloproteases in the early- and late-phase development of neuropathic painNature Medicine, 2008
- Interleukin‐1‐induced interleukin‐6 synthesis is mediated by the neutral sphingomyelinase/Src kinase pathway in neuronesBritish Journal of Pharmacology, 2008
- CNS‐infiltrating CD4+ T lymphocytes contribute to murine spinal nerve transection‐induced neuropathic painEuropean Journal of Immunology, 2008
- “Listening” and “talking” to neurons: Implications of immune activation for pain control and increasing the efficacy of opioidsBrain Research Reviews, 2007
- Quantification of the rat spinal microglial response to peripheral nerve injury as revealed by immunohistochemical image analysis and flow cytometryJournal of Neuroscience Methods, 2007
- Role of the CX3CR1/p38 MAPK pathway in spinal microglia for the development of neuropathic pain following nerve injury-induced cleavage of fractalkineBrain, Behavior, and Immunity, 2007
- The chemokine CX3CL1/fractalkine interferes with the antinociceptive effect induced by opioid agonists in the periaqueductal grey of ratsBrain Research, 2007
- Possible role of spinal astrocytes in maintaining chronic pain sensitization: review of current evidence with focus on bFGF/JNK pathwayNeuron Glia Biology, 2006
- Purinergic signalling in neuron–glia interactionsNature Reviews Neuroscience, 2006