Astrocyte albumin-induced activation. (IMAGE)
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Intracellular Ca2+ waves and K+ accumulation are crucial causative factors contributing to the dysfunction of the astrocyte network. Both endothelial cells and the activation of mGluR5 can exacerbate the levels of Ca2+ within astrocytes. Elevated intracellular Ca2+ levels promote the calcium-dependent release of glutamate and the release of ATP (adenosine triphosphate)from the cell into the extracellular space. The downregulation of Kir channels in activated astrocytes leads to an inadequate K+ buffering capacity, while extracellular K+ levels decrease the expression of EAAT(excitatory amino acid transporter) proteins. This ultimately results in a high concentration of extracellular K+ and glutamate. Additionally, GJ proteins are influenced by changes in K+ levels and pH. Due to alterations in the extracellular environment, GJ proteins exhibit functional abnormalities, leading not only to disruptions in the astrocyte network but also triggering further K+ release. This, in turn, affects the normal functioning of synapses, ultimately contributing to the onset of epilepsy. Glutamate receptor channels remain the primary candidates responsible for generating the large inward currents that give rise to anoxic depolarization.
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