Abstract
Neurons and glial cells maintain a steep inwardly directed electrochemical gradient for Na+ across their plasma membranes. This gradient is provided by Na +, K+-ATPase activity and energizes a multitude of transmembrane processes. Recent investigations have sug gested that sustained increases in Na+i, following inhibition of Na+, K+-ATPase, or Na+ influx via voltage- or transmitter-activated ion channels, are key events during a variety of pathological conditions. Breakdown of the Na+ gradient causes reverse operation of Na+/Ca2+- and Na+/H+-exchange, resulting in intracellular Ca2+ increase and acidification. In addition, reversal of Na +-dependent glutamate transport promotes glutamate export, which can result in toxic glutamate concentrations in the extracellular space. Further stud ies of the mechanisms of Na+i regulation in neurons and glial cells may provide more insights into events initiating cell damage in the nervous system. NEUROSCIENTIST 3:85-88, 1997