Deficient KCC2 activity has been described following neuronal damage such as physical trauma or ischemia and the following mechanisms are suggested to be involved: transcriptional regulation via neurotrophin receptor activation (Rivera et al., 2002, 2004), post-translational regulation via changes in the phosphorylation state of KCC2 (Blaesse et al., 2009; Chamma et al., 2013) and activity-dependent down-regulation after NMDA-receptor activation and calcium influx (Ginsberg, 2008; Lee et al., 2011). This evidence concerns the gene SLC12A5 and ischemia.