期刊
TRENDS IN NEUROSCIENCES
卷 36, 期 12, 页码 726-737出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2013.08.006
关键词
-
资金
- Letten Foundation
- Academy of Finland
- Sigrid Juselius Foundation
- Jane and Aatos Erkko Foundation
- National Institutes of Health
- Simons Foundation Autism Research Initiative
- Manton Center for Orphan Disease Research
- Congress of Neurological Surgeons
The K-CI cotransporter KCC2 establishes the low intraneuronal Cl- levels required for the hyperpolarizing inhibitory postsynaptic potentials mediated by ionotropic gamma-aminobutyric acid receptors (GABA(A)Rs) and glycine receptors (GlyRs). Decreased KCC2-mediated Cl- extrusion and impaired hyperpolarizing GABA(A)R- and/or GlyR-mediated currents have been implicated in epilepsy, neuropathic pain, and spasticity. Recent evidence suggests that the intrinsic ion transport rate, cell surface stability, and plasmalemmal trafficking of KCC2 are rapidly and reversibly modulated by the (de)phosphorylation of critical serine, threonine, and tyrosine residues in the C terminus of this protein. Alterations in KCC2 phosphorylation have been associated with impaired KCC2 function in several neurological diseases. Targeting KCC2 phosphorylation directly or indirectly via upstream regulatory kinases might be a novel strategy to modulate GABA- and/or glycinergic signaling for therapeutic benefit.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据