The mechanism involves Kir4.1 that facilitates the clearance of extracellular potassium (K+), leading to a decrease in extracellular K+ concentration, which directly influences the resting membrane potassium (RMP) of neurons, leading to hyperpolarization of neurons, and activates calcium channels that promote bursting, ultimately affecting monoaminergic centers involved in the pathophysiology of depression [150]. Here, KCNJ10 is linked to depressive symptom measurement.