Neuronal inhibition is critically dependent on K+/Cl− transporter (KCC2) activity, which helps maintain low intracellular Cl− levels. Now, a new mouse study has shown that KCC2 could be a key regulator of the onset and severity of status epilepticus. Phosphorylation of KCC2 at Ser940 enhances KCC2 function in vivo, and kainate-induced seizures result in rapid Ser940 dephosphorylation and subsequent loss of neuronal Cl− homeostasis. Previous genetic studies have reported KCC2 mutations that decrease Ser940 phosphorylation in humans with idiopathic epilepsy, suggesting that modulation of KCC2 activity might have therapeutic potential.
References
Silayeva, L. et al. KCC2 activity is critical in limiting the onset and severity of status epilepticus. Proc. Natl Acad. Sci. USA 10.1073/pnas.1415126112
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KCC2 phosphorylation is critical for limiting the severity of status epilepticus in mice. Nat Rev Neurol 11, 185 (2015). https://doi.org/10.1038/nrneurol.2015.41
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DOI: https://doi.org/10.1038/nrneurol.2015.41
