Endocrine Abstracts

Ca²+ homeostasis has been reported to play important roles in various cell systems. In central nerves system, the dysregulation of Ca²+ homeostasis can induce the excitotoxic and neurodegeneration. NCKX3 (Sodium/potassium/calcium exchanger 3), a novel member of the family of K+-dependent Na+/Ca²+ exchangers, is an important component of intracellular Ca²+ homeostasis. In addition, NCKX3 highly expressed in thalamic nuclei, in hippocampal CA1 neurons, and in layer IV of the cerebral cortex in the mouse brain. Here, we examined the effects of inactivation of NCKX3 in mice. NCKX3 deficient mice at 6 week-age were used for behavior assays. In comparison to wild-type (WT) mice, NCKX3 deficient mice displayed hyperactivity in the open field test. In addition, the rotarod test revealed motor learning defects in NCKX3 knock out (KO) mice. Moreover, NCKX3 deficient mice have reduced time spent on general sniffing, anogenital sniffing, and following behavior in social interaction test compared to WT mice. In three-chamber social ability test, NCKX3 deficient mice showed spent more time in the chamber contain un-familiar mouse. However, NCKX3 deficient mice exhibited significantly lower time spent in the novel mice in social novel test. NCKX3 deficient mice showed no change in cognition function in the novel object recognition and spatial learning in Morris water maze tests. These results indicated that NCKX3 mutation causes abnormal motor functions and social behaviors in mice.