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Intracellular Na+ Regulation in Neurons and Glia: Functional Implications

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

Key Words: KEY WORDS Sodium • Na+ • K+-ATPase • Na+/Ca2+ exchanger • Na+ channels • SBFI

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