|
| | | | |
| | | |
| Stat |
Members: 3645
Articles: 2'500'096
Articles rated: 2609
18 April 2024 |
|
| | | | |
|
Article overview
| |
|
|
Trans-synaptic shift in anion gradient in spinal lamina I neurons as a mechanism of neuropathic pain | | Jeffrey A M Coull
; Dominic Boudreau
; Karine Bach
; Steven A Prescott
; Francine Nault
; Attila Sík
; Paul De Koninck
; Yves De Koninck
; | | Date: |
21 Aug 2003 | | Journal: | Nature, 424 (6951), 938-42 | | Abstract: | Modern pain-control theory predicts that a loss of inhibition (disinhibition) in the dorsal horn of the spinal cord is a crucial substrate for chronic pain syndromes. However, the nature of the mechanisms that underlie such disinhibition has remained controversial. 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 pathways. 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. | | Source: | PubMed, pmid12931188 doi: 10.1038/nature01868 | | Services: | Forum | Review | Favorites | |
|
|
No review found.
Did you like this article?
Note: answers to reviews or questions about the article must be posted in the forum section.
Authors are not allowed to review their own article. They can use the forum section.
browser claudebot
|
| |
|
|
|
|
News, job offers and information for researchers and scientists:
| |
REGISTER