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

Marzia Malcangio

doi:10.1016/j.ynpai.2017.04.001

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

Marzia Malcangio

Research output: Contribution to journal › Short survey › peer-review

20 Citations (Scopus)

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.

Original language	English
Pages (from-to)	1-5
Number of pages	5
Journal	Neurobiology of Pain
Volume	1
Early online date	17 May 2017
DOIs	https://doi.org/10.1016/j.ynpai.2017.04.001
Publication status	E-pub ahead of print - 17 May 2017

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10.1016/j.ynpai.2017.04.001

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title = "Spinal mechanisms of neuropathic pain: Is there a P2X4-BDNF controversy?",

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

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