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2 vity of a bumetanide-sensitive NKCC1 (sodium potassium chloride cotransporter 1)-like chloride cotran
3 t CA1 pyramidal neurons because of increased potassium chloride cotransporter 2 (KCC2) expression and
4 ride shift caused by significant decrease in potassium chloride cotransporter 2 (Kcc2) mRNA expressio
6 y gamma-aminobutyric acid and glycine due to potassium chloride cotransporter-2 (KCC2) down-regulatio
8 s of Tbx1 or Slc12a2, which encodes a sodium-potassium-chloride cotransporter and is also necessary f
9 s associated with reduced dorsal spinal cord potassium chloride cotransporter expression and impaired
10 ction is downregulated, including the sodium-potassium-chloride cotransporter gene nkcc1 (slc12a2) an
16 w that specific markers of excitability, the potassium-chloride cotransporter KCC2 and GABAA receptor
17 n associated with dysfunction or loss of the potassium-chloride cotransporter KCC2 in a subset of pyr
18 decrease in the functional expression of the potassium-chloride cotransporter KCC2 in spinal cord dor
23 (hepatocyte nuclear factor 4alpha), SLC12A5 (potassium-chloride cotransporter member 5), CDH22 (cadhe
24 receptors can physically associate with the potassium-chloride cotransporter protein, KCC2, which se
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