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Abstract
Calcium-dependent inactivation (CDI) is an important mechanism that is common to a variety of ion channels, and is particularly important to the function of the N-methyl-D-aspartic acid (NMDA) receptor (1,2). The NMDA receptor is a class of glutamate receptor that is a mediator of synaptic plasticity and has been a target for neurological drug development. In particular, spike timing-dependent plasticity is thought to be influenced by CDI (3). CDI is mediated by the interaction of calmodulin with a sequence on the intracellular C-terminal domain (C0) of the NMDA receptor 1 (NR1) subunit of the NMDA receptor (4) and by the binding of calcium to calmodulin.
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