Sodium dynamics: another key to astroglial excitability?
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Updated: May 22, 2026

Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates
Published on: March 20, 2014
Sergei Kirischuk1, Vladimir Parpura, Alexei Verkhratsky
1Institute of Physiology and Pathophysiology, Universal Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Abstract:
Astroglial excitability is largely mediated by fluctuations in intracellular ion concentrations. In addition to generally acknowledged Ca²⁺ excitability of astroglia, recent studies have demonstrated that neuronal activity triggers transient increases in the cytosolic Na⁺ concentration ([Na⁺](i)) in perisynaptic astrocytes. These [Na⁺](i) transients are controlled by multiple Na⁺-permeable channels and Na⁺-dependent transporters; spatiotemporally organized [Na⁺](i) dynamics in turn regulate diverse astroglial homeostatic responses such as metabolic/signaling utilization of lactate and glutamate, transmembrane transport of neurotransmitters and K⁺ buffering. In particular, near-membrane [Na⁺](i) transients determine the rate and the direction of the transmembrane transport of GABA and Ca²⁺. We discuss here the role of Na⁺ in the regulation of various systems that mediate fast bidirectional communication between neurones and glia at the single synapse level.
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Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential.
Glial Cells

