Glial ER and GAP junction mediated Ca 2+ waves are crucial to maintain normal brain excitability
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 neu...
| Principais autores: | , , , , , |
|---|---|
| Outros Autores: | |
| Formato: | Artigo |
| Idioma: | English |
| Publicado em: |
Wiley
2022
|
| Acesso em linha: | https://hdl.handle.net/1721.1/146892 |
| _version_ | 1826201745263427584 |
|---|---|
| author | Weiss, Shirley Clamon, Lauren C Manoim, Julia E Ormerod, Kiel G Parnas, Moshe Littleton, J Troy |
| author2 | Massachusetts Institute of Technology. Department of Biology |
| author_facet | Massachusetts Institute of Technology. Department of Biology Weiss, Shirley Clamon, Lauren C Manoim, Julia E Ormerod, Kiel G Parnas, Moshe Littleton, J Troy |
| author_sort | Weiss, Shirley |
| collection | MIT |
| description | 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. |
| first_indexed | 2024-09-23T11:56:26Z |
| format | Article |
| id | mit-1721.1/146892 |
| institution | Massachusetts Institute of Technology |
| language | English |
| last_indexed | 2024-09-23T11:56:26Z |
| publishDate | 2022 |
| publisher | Wiley |
| record_format | dspace |
| spelling | mit-1721.1/1468922022-12-16T03:27:34Z Glial ER and GAP junction mediated Ca 2+ waves are crucial to maintain normal brain excitability Weiss, Shirley Clamon, Lauren C Manoim, Julia E Ormerod, Kiel G Parnas, Moshe Littleton, J Troy Massachusetts Institute of Technology. Department of Biology 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. 2022-12-15T18:54:59Z 2022-12-15T18:54:59Z 2022 2022-12-15T18:37:59Z Article http://purl.org/eprint/type/JournalArticle https://hdl.handle.net/1721.1/146892 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). en 10.1002/GLIA.24092 Glia Creative Commons Attribution-Noncommercial-Share Alike http://creativecommons.org/licenses/by-nc-sa/4.0/ application/pdf Wiley PMC |
| spellingShingle | Weiss, Shirley Clamon, Lauren C Manoim, Julia E Ormerod, Kiel G Parnas, Moshe Littleton, J Troy Glial ER and GAP junction mediated Ca 2+ waves are crucial to maintain normal brain excitability |
| title | Glial ER and GAP junction mediated Ca 2+ waves are crucial to maintain normal brain excitability |
| title_full | Glial ER and GAP junction mediated Ca 2+ waves are crucial to maintain normal brain excitability |
| title_fullStr | Glial ER and GAP junction mediated Ca 2+ waves are crucial to maintain normal brain excitability |
| title_full_unstemmed | Glial ER and GAP junction mediated Ca 2+ waves are crucial to maintain normal brain excitability |
| title_short | Glial ER and GAP junction mediated Ca 2+ waves are crucial to maintain normal brain excitability |
| title_sort | glial er and gap junction mediated ca 2 waves are crucial to maintain normal brain excitability |
| url | https://hdl.handle.net/1721.1/146892 |
| work_keys_str_mv | AT weissshirley glialerandgapjunctionmediatedca2wavesarecrucialtomaintainnormalbrainexcitability AT clamonlaurenc glialerandgapjunctionmediatedca2wavesarecrucialtomaintainnormalbrainexcitability AT manoimjuliae glialerandgapjunctionmediatedca2wavesarecrucialtomaintainnormalbrainexcitability AT ormerodkielg glialerandgapjunctionmediatedca2wavesarecrucialtomaintainnormalbrainexcitability AT parnasmoshe glialerandgapjunctionmediatedca2wavesarecrucialtomaintainnormalbrainexcitability AT littletonjtroy glialerandgapjunctionmediatedca2wavesarecrucialtomaintainnormalbrainexcitability |