Key result
NCKX2 knockout in mice reduces cortical Ca2+ flux, impairing motor learning and spatial memory.
NCKX2 plays a critical and non-redundant role in the local control of neuronal calcium homeostasis essential for synaptic plasticity, learning, and memory.
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NCKX2 is essential for synaptic plasticity and memory in mice; leaves open its relevance to human cognitive disorders.
Plasma membrane Na+/Ca2+-exchangers play a predominant role in Ca2+ extrusion in brain. Neurons express several different Na+/Ca2+-exchangers belonging to both the K+-independent NCX family and the K+-dependent NCKX family. The unique contributions of each of these proteins to neuronal Ca2+ homeostasis and/or physiology remain largely unexplored. To address this question, we generated mice in which the gene encoding the abundant neuronal K+ -dependent Na+/Ca2+-exchanger protein, NCKX2, was knocked out. Analysis of these animals revealed a significant reduction in Ca2+ flux in cortical neurons, a profound loss of long term potentiation and an increase in long term depression at hippocampal Schaffer/CA1 synapses, and clear deficits in specific tests of motor learning and spatial working memory. Surprisingly, there was no obvious loss of photoreceptor function in cones, where expression of the NCKX2 protein had been reported previously. These data emphasize the critical and non-redundant role of NCKX2 in the local control of neuronal [Ca2+] that is essential for the development of synaptic plasticity associated with learning and memory.
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Li et al. (2006) studied Motor learning and memory. NCKX2 gene knockout vs. Wild-type was evaluated on Ca2+ flux, long term potentiation, long term depression, motor learning, and spatial working memory. NCKX2 knockout in mice resulted in reduced cortical neuron Ca2+ flux, loss of long-term potentiation, increased long-term depression, and deficits in motor learning and spatial working memory.
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