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Spinal mechanisms of neuropathic pain: Is there a P2X4-BDNF controversy?

Research output: Contribution to journalShort surveypeer-review

Original languageEnglish
Pages (from-to)1-5
Number of pages5
JournalNeurobiology of Pain
Volume1
Early online date17 May 2017
DOIs
Accepted/In press7 Apr 2017
E-pub ahead of print17 May 2017

King's Authors

Abstract

More than a decade ago the novel concept that glial cells are major players in the modulation of pain mechanisms in the spinal cord has started a prolific series of work addressing the modalities of neuron-glia communication. Mike Salter with Kazuhide Inoue laboratories introduced ATP as pivotal mediator for such communication via activation of P2X4 receptors expressed by microglia in the dorsal horn ipsilateral to a peripheral nerve injury. Activation of P2X4 receptors result in release of the neurotrophin BDNF, which, through the activation of neuronal TrkB receptors, alters neuronal excitability and this effect is associated with behavioural ipsilateral allodynia. This viewpoint article compares the evidence supporting a biological relevance of the P2X4 and BDNF system in neuropathic pain with recent data which question such importance. Having read this article, readers will be able to formulate their own opinion on such controversy.

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