Neuron-glia crosstalk gets serious: role in pain hypersensitivity.
Neuron-glia crosstalk gets serious: role in pain hypersensitivity.
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DOI:
10.1097/aco.0b013e32830edbdf
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发表时间:
2008-10
期刊:
影响因子:
--
通讯作者:
Dubner R
中科院分区:
文献类型:
--
作者:
Ren K;Dubner R
Recent studies show that peripheral injury activates both neuronal and non-neuronal or glial components of the peripheral and central cellular circuitry. The subsequent neuron-glial interactions contribute to pain hypersensitivity. This review will briefly discuss novel findings that have shed light on the cellular mechanisms of neuron-glial interactions in persistent pain. Two fundamental questions related to neuron-glial interactions in pain mechanisms have been addressed: 1) what are the signals that lead to central glial activation after injury and 2) how glial cells affect CNS neuronal activity and promote hyperalgesia. 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/infiltrate to the brain and circulating inflammatory mediators may penetrate the blood brain barrier to participate in central glial responses to injury. Inflammatory cytokines such as IL-1β released from glia may facilitate pain transmission through its coupling to neuronal glutamate receptors. This bidirectional neuron-glial 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-glial interactions to central sensitization and hyperalgesia prompts new treatment for chronic pain.