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Role of NKCC1 and KCC2 in the development of chronic neuropathic pain following spinal cord injury.
- Source :
-
Annals of the New York Academy of Sciences . Jun2010, Vol. 1198 Issue 1, p168-172. 5p. 1 Black and White Photograph, 1 Diagram, 1 Graph. - Publication Year :
- 2010
-
Abstract
- Neuropathic pain is a common problem following spinal cord injury (SCI). Effective analgesic therapy has been hampered by the lack of knowledge about the mechanisms underlying post-SCI neuropathic pain. Current evidence suggests GABAergic spinal nociceptive processing is a critical functional node in this complex phenotype, representing a potential target for therapeutic intervention. Normal GABA neurotransmission is dependent on precise regulation of the level of intracellular chloride, which is determined by the coordinated activities of two cation/chloride cotransporters (CCCs) in the SLC12 family: the inwardly directed Na+-K+-Cl− cotransporter isoform 1 (NKCC1) and outwardly directed K+-Cl− cotransporter isoform 2 (KCC2). Inhibition of NKCC1 with its potent antagonist bumetanide reduces pain behavior in rats following SCI. Moreover, the injured spinal cord tissues exhibit a significant transient upregulation of NKCC1 protein and a concurrent downregulation of KCC2 protein. Thus, imbalanced function of NKCC1 and KCC2 may contribute to the induction and maintenance of the chronic neuropathic pain following SCI. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00778923
- Volume :
- 1198
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Annals of the New York Academy of Sciences
- Publication Type :
- Academic Journal
- Accession number :
- 51325407
- Full Text :
- https://doi.org/10.1111/j.1749-6632.2010.05462.x