Glial ER and GAP junction mediated Ca 2+ waves are crucial to maintain normal brain excitability
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nihms-1796234.pdf
Description
Accepted version
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3.09 MB
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Checksum (MD5)
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Author(s)
Weiss, Shirley
Clamon, Lauren C
Manoim, Julia E
Ormerod, Kiel G
Parnas, Moshe
Littleton, J Troy
Date Issued
2022
Journal
Glia
Publisher
Wiley
Citation
Weiss, Shirley, Clamon, Lauren C, Manoim, Julia E, Ormerod, Kiel G, Parnas, Moshe et al. 2022. "Glial ER and GAP junction mediated Ca 2+ waves are crucial to maintain normal brain excitability." Glia, 70 (1).
Version
Author's final manuscript
Abstract
Astrocytes play key roles in regulating multiple aspects of neuronal function from invertebrates to humans and display Ca2+ fluctuations that are heterogeneously distributed throughout different cellular microdomains. Changes in Ca2+ dynamics represent a key mechanism for how astrocytes modulate neuronal activity. An unresolved issue is the origin and contribution of specific glial Ca2+ signaling components at distinct astrocytic domains to neuronal physiology and brain function. The Drosophila model system offers a simple nervous system that is highly amenable to cell-specific genetic manipulations to characterize the role of glial Ca2+ signaling. Here we identify a role for ER store-operated Ca2+ entry (SOCE) pathway in perineurial glia (PG), a glial population that contributes to the Drosophila blood-brain barrier. We show that PG cells display diverse Ca2+ activity that varies based on their locale within the brain. Ca2+ signaling in PG cells does not require extracellular Ca2+ and is blocked by inhibition of SOCE, Ryanodine receptors, or gap junctions. Disruption of these components triggers stimuli-induced seizure-like episodes. These findings indicate that Ca2+ release from internal stores and its propagation between neighboring glial cells via gap junctions are essential for maintaining normal nervous system function.
MIT Department
Massachusetts Institute of Technology. Department of Biology
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Creative Commons Attribution-Noncommercial-Share Alike
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DOI of Published Version
https://doi.org/10.1002/GLIA.24092
