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- W2171661590 abstract "GABA-mediated fast-hyperpolarizing inhibition depends on extrusion of chloride by the neuron-specific K-Cl cotransporter, KCC2. Here we show that sustained interictal-like activity in hippocampal slices downregulates KCC2 mRNA and protein expression in CA1 pyramidal neurons, which leads to a reduced capacity for neuronal Cl- extrusion. This effect is mediated by endogenous BDNF acting on tyrosine receptor kinase B (TrkB), with down-stream cascades involving both Shc/FRS-2 (src homology 2 domain containing transforming protein/FGF receptor substrate 2) and PLCgamma (phospholipase Cgamma)-cAMP response element-binding protein signaling. The plasmalemmal KCC2 has a very high rate of turnover, with a time frame that suggests a novel role for changes in KCC2 expression in diverse manifestations of neuronal plasticity. A downregulation of KCC2 may be a general early response involved in various kinds of neuronal trauma." @default.
- W2171661590 created "2016-06-24" @default.
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- W2171661590 date "2004-05-12" @default.
- W2171661590 modified "2023-10-14" @default.
- W2171661590 title "Mechanism of Activity-Dependent Downregulation of the Neuron-Specific K-Cl Cotransporter KCC2" @default.
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- W2171661590 doi "https://doi.org/10.1523/jneurosci.5265-03.2004" @default.
- W2171661590 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6729393" @default.
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