Endocrine Abstracts

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. 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 NCKX3 deletion in mice. NCKX3 knockout (KO) mice at 6 week-age were used for behavior assays. NCKX3 KO mice show increased moving distances in the open field test. In the sociability test, NCKX3 KO mice have reduced time spent on general sniffing, anogenital sniffing, and following behavior but increased in fighting. Additionally, the rotarod test revealed motor learning defects in NCKX3 KO mice. However, NCKX3 KO mice showed 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 KO mice. This indicated NCKX3 mutation did not impair to spatial learning in mice. These results suggest that NCKX3 mutation causes abnormal motor functions and social behaviors in mice.