The Na+/K+-ATPase is a transmembrane protein acting as an electrogenic Na+ and K+ transporter in the plasma membrane of all mammalian cells. Although the Na+/K+-ATPase was first discovered in neuronal tissue, its function has been more extensively characterized in cardiac and renal tissues, and the Na+/K+-ATPase has emerged as a novel drug target in these systems. This review will focus on the function and dysfunction of the plasma membrane Na+/K+-ATPase in the context of neuronal diseases. More specifically, we will outline the structure, function, and regulation of the Na+/K+-ATPase under normal as well as hypoxic/ischemic conditions. We will review recent evidence on the relationship between the Na+/K+-ATPase and K+ homeostasis in neuronal apoptosis, outline the emerging role of ouabain and other Na+/K+-ATPase inhibitors as endogenous hormones which activate specific signal transduction cascades by binding to the Na+/K+-ATPase, and evaluate the impact of these signal transduction functions on the role of Na+/K+-ATPase in CNS diseases.
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