NCKX3 (sodium/potassium/calcium exchanger 3) is an important component of intracellular Ca2+ homeostasis. Ca2+ homeostasis has been extensively studied in various cell systems. Dysregulation of Ca2+ homeostasis can induce the excitotoxic and neurodegeneration in central nervous system. NCKX3 gene is 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. Mice lacking NCKX3 at 6 week-age were used for behavior assays. NCKX3‑/- mice show increased moving distances in the open field test. In the sociability test, NCKX3-/- mice have reduced time spent on general sniffing, anogenital sniffing, and following behavior but increased in fighting. In the rotarod test, there were abnormal in motor learnings in NCKX3-/- mice. There was no change in recognition memory in the novel object recognition test. During acquisition phase in the Morris water maze test, there was no different in escape latency time between wild-type and NCKX3-/- mice. This indicated NCKX3 mutation did not impair to spatial learning in mice. The data show an essential in vivo role for NCKX3 in motor functions and social behaviors in mice.
This work was supported by the National Research Foundation of Korea (NRF) grant of Korean government (MEST) (No. 2015R1A6A1A04020885)