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By maintaining ionic balance, neurotransmitter turnover, and metabolic support, they sustain neuronal excitability and network stability. Ionic excitability of astrocytes is mediated primarily by fluctuations of intracellular Na\n                    <jats:sup>+<\/jats:sup>\n                    , K\n                    <jats:sup>+<\/jats:sup>\n                    , Ca\n                    <jats:sup>2+<\/jats:sup>\n                    , and Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    ions. Central to these processes is the Na\n                    <jats:sup>+<\/jats:sup>\n                    ,K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase, which maintains transmembrane Na\n                    <jats:sup>+<\/jats:sup>\n                    and K\n                    <jats:sup>+<\/jats:sup>\n                    gradients, driving secondary active transport, including uptake of neurotransmitters such as glutamate, \u03b3-aminobutyric acid, and their precursors glutamine and L-serine. Astrocytic Na\n                    <jats:sup>+<\/jats:sup>\n                    changes rapidly coordinate neuronal activity with glial homeostasis via N-methyl-d-aspartate receptor signaling, whereas K\n                    <jats:sup>+<\/jats:sup>\n                    clearance is primarily mediated by the Na\n                    <jats:sup>+<\/jats:sup>\n                    ,K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase \u03b1\n                    <jats:sub>2<\/jats:sub>\n                    isoform, preventing neuronal hyperexcitability. The Na\n                    <jats:sup>+<\/jats:sup>\n                    ,K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase also contributes to neurovascular coupling, linking synaptic activity to local vasodilation through Ca\n                    <jats:sup>2+<\/jats:sup>\n                    - and K\n                    <jats:sup>+<\/jats:sup>\n                    -dependent signaling in astrocytic endfeet. Beyond ion transport, the Na\n                    <jats:sup>+<\/jats:sup>\n                    ,K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase serves as a signaling hub, engaging intracellular kinase signaling pathways, including Src and phosphoinositide 3-kinase kinases, thereby modulating astrocyte morphology, metabolism, and stress responses. Dysfunctions of astrocytic Na\n                    <jats:sup>+<\/jats:sup>\n                    ,K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase isoforms are implicated in multiple neuronal pathologies, including seizures, familial hemiplegic migraine, neurodegeneration, and neuroinflammatory disorders. These pathologies reflect primarily loss-of-function mechanisms, altered ion homeostasis, and reactive oxygen species or inflammatory signaling. Understanding the isoform- and cell-type-specific functions of the Na\n                    <jats:sup>+<\/jats:sup>\n                    ,K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase across the neurovascular unit will be crucial for future development of targeted therapies aimed to restore ion homeostasis and signaling in the diseased brain.\n                  <\/jats:p>","DOI":"10.1152\/ajpcell.00814.2025","type":"journal-article","created":{"date-parts":[[2025,12,9]],"date-time":"2025-12-09T15:21:46Z","timestamp":1765293706000},"page":"C238-C251","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":6,"title":["The astrocytic engine: Na\n                    <sup>+<\/sup>\n                    ,K\n                    <sup>+<\/sup>\n                    -ATPase at the nexus of brain function and 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