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• W2059952163 abstract "Neuroglial cells are homeostatic neural cells. Generally, they are electrically non-excitable and their activation is associated with the generation of complex intracellular Ca(2+) signals that define the Ca(2+) excitability of glia. In mammalian glial cells the major source of Ca(2+) for this excitability is the lumen of the endoplasmic reticulum (ER), which is ultimately (re)filled from the extracellular space. This occurs via store-operated Ca(2+) entry (SOCE) which is supported by a specific signaling system connecting the ER with plasmalemmal Ca(2+) entry. Here, emptying of the ER Ca(2+) store is necessary and sufficient for the activation of SOCE, and without Ca(2+) influx via SOCE the ER store cannot be refilled. The molecular arrangements underlying SOCE are relatively complex and include plasmalemmal channels, ER Ca(2+) sensors, such as stromal interaction molecule, and possibly ER Ca(2+) pumps (of the SERCA type). There are at least two sets of plasmalemmal channels mediating SOCE, the Ca(2+)-release activated channels, Orai, and transient receptor potential (TRP) channels. The molecular identity of neuroglial SOCE has not been yet identified unequivocally. However, it seems that Orai is predominantly expressed in microglia, whereas astrocytes and oligodendrocytes rely more on TRP channels to produce SOCE. In physiological conditions the SOCE pathway is instrumental for the sustained phase of the Ca(2+) signal observed following stimulation of metabotropic receptors on glial cells." @default.
• W2059952163 created "2016-06-24" @default.
• W2059952163 creator A5016152202 @default.
• W2059952163 creator A5083227570 @default.
• W2059952163 date "2013-05-15" @default.
• W2059952163 modified "2023-09-26" @default.
• W2059952163 title "Store-operated calcium entry in neuroglia" @default.
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• W2059952163 doi "https://doi.org/10.1007/s12264-013-1343-x" @default.
• W2059952163 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5561850" @default.
• W2059952163 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23677809" @default.
• W2059952163 hasPublicationYear "2013" @default.
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