Trans-synaptic shift in anion gradient in spinal lamina I neurons as a mechanism of neuropathic pain View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2003-08

AUTHORS

Jeffrey A. M. Coull, Dominic Boudreau, Karine Bachand, Steven A. Prescott, Francine Nault, Attila Sík, Paul De Koninck, Yves De Koninck

ABSTRACT

Modern pain-control theory1 predicts that a loss of inhibition (disinhibition) in the dorsal horn of the spinal cord is a crucial substrate for chronic pain syndromes2. However, the nature of the mechanisms that underlie such disinhibition has remained controversial3,4,5,6. Here we present evidence for a novel mechanism of disinhibition following peripheral nerve injury. It involves a trans-synaptic reduction in the expression of the potassium–chloride exporter KCC2, and the consequent disruption of anion homeostasis in neurons of lamina I of the superficial dorsal horn, one of the main spinal nociceptive output pathways7. In our experiments, the resulting shift in the transmembrane anion gradient caused normally inhibitory anionic synaptic currents to be excitatory, substantially driving up the net excitability of lamina I neurons. Local blockade or knock-down of the spinal KCC2 exporter in intact rats markedly reduced the nociceptive threshold, confirming that the reported disruption of anion homeostasis in lamina I neurons was sufficient to cause neuropathic pain. More... »

PAGES

938-942

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature01868

DOI

http://dx.doi.org/10.1038/nature01868

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1042146459

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/12931188


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