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• W2054687577 startingPage "17404" @default.
• W2054687577 abstract "Astrocytes in hippocampal slices can dynamically regulate synaptic transmission in a process mediated by increases in intracellular Ca 2+ . However, it is debated whether astrocytic Ca 2+ signals result in release of glutamate. We here compared astrocytic Ca 2+ signaling triggered by agonist exposure versus photolysis side by side. Using transgenic mice in which astrocytes selectively express the MrgA1 receptor, we found that receptor-mediated astrocytic Ca 2+ signaling consistently triggered neuronal hyperpolarization and decreased the frequency of miniature excitatory postsynaptic currents (EPSCs). In contrast, photolysis of caged Ca 2+ ( o -nitrophenyl–EGTA) in astrocytes led to neuronal depolarization and increased the frequency of mEPSCs through a metabotropic glutamate receptor-mediated pathway. Analysis of transgenic mice in which astrocytic vesicular release is suppressed (dominant-negative SNARE mice) and pharmacological manipulations suggested that glutamate is primarily released by opening of anion channels rather than exocytosis. Combined, these studies show that photolysis but not by agonists induced astrocytic Ca 2+ signaling triggers glutamate release." @default.
• W2054687577 created "2016-06-24" @default.
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• W2054687577 date "2013-10-30" @default.
• W2054687577 modified "2023-10-01" @default.
• W2054687577 title "Photolysis of Caged Ca²⁺But Not Receptor-Mediated Ca²⁺Signaling Triggers Astrocytic Glutamate Release" @default.
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• W2054687577 doi "https://doi.org/10.1523/jneurosci.2178-13.2013" @default.
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