BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain

Jeffrey A. M. Coull, Simon Beggs, Dominic Boudreau, Dominick Boivin, Makoto Tsuda, Kazuhide Inoue, Claude Gravel, Michael W. Salter () and Yves De Koninck ()
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Jeffrey A. M. Coull: Centre de Recherche Université Laval Robert-Giffard
Simon Beggs: The Hospital for Sick Children
Dominic Boudreau: Centre de Recherche Université Laval Robert-Giffard
Dominick Boivin: Centre de Recherche Université Laval Robert-Giffard
Makoto Tsuda: The Hospital for Sick Children
Kazuhide Inoue: Kyushu University
Claude Gravel: Centre de recherche Université Laval Robert-Giffard
Michael W. Salter: The Hospital for Sick Children
Yves De Koninck: Centre de Recherche Université Laval Robert-Giffard

Nature, 2005, vol. 438, issue 7070, 1017-1021

Abstract: GABA is a pain Neuropathic pain, one of the most debilitating of all pain states, often arises from injury to a peripheral nerve that depends on activation of a specific cell type known as microglia. This prompts the question, how do the microglia signal to spinal pain neurons? Coull et al. have now identified the biophysical mechanism by which microglia, activated by ATP, cause hyperexcitability of spinal neurons. The microglia release brain-derived neurotrophic factor, which alters chloride ion distribution across the plasma membrane of neurons in lamina I of the spinal cord. This results in the neurotransmitter, GABA, activating (rather than inhibiting) these cells that form part of a major pathway that signals pain. A collection of recent reprints on neuropathic pain, taken from Nature Publishing Group journals is, now available online via tinyurl.com/dzw86.

Date: 2005
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DOI: 10.1038/nature04223

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