KCNJ10 and Cohen syndrome: Our previous studies demonstrated that Kir currents, especially Kir4.1-mediated ones, and Kir4.1 proteins in Müller cells showed a significant reduction in a rat chronic ocular hypertension (COH) model due to over-activated group I metabotropic glutamate receptors (mGluR I) by excessive extracellular glutamate, which contributes to Müller cell gliosis11.