Multiscale Modeling Indicates That Temperature Dependent [Ca2+]i Spiking in Astrocytes Is Quantitatively Consistent with Modulated SERCA Activity
Changes in the cytosolic Ca2+ concentration ([Ca2+]i) are the most predominant active signaling mechanism in astrocytes that can modulate neuronal activity and is assumed to influence neuronal plasticity. Although Ca2+ signaling in astrocytes has been intensively studied in the past, our understandi...
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Format: | Article |
Language: | English |
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Wiley
2015-01-01
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Series: | Neural Plasticity |
Online Access: | http://dx.doi.org/10.1155/2015/683490 |
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author | Niko Komin Mahsa Moein Mark H. Ellisman Alexander Skupin |
author_facet | Niko Komin Mahsa Moein Mark H. Ellisman Alexander Skupin |
author_sort | Niko Komin |
collection | DOAJ |
description | Changes in the cytosolic Ca2+ concentration ([Ca2+]i) are the most predominant active signaling mechanism in astrocytes that can modulate neuronal activity and is assumed to influence neuronal plasticity. Although Ca2+ signaling in astrocytes has been intensively studied in the past, our understanding of the signaling mechanism and its impact on tissue level is still incomplete. Here we revisit our previously published data on the strong temperature dependence of Ca2+ signals in both cultured primary astrocytes and astrocytes in acute brain slices of mice. We apply multiscale modeling to test the hypothesis that the temperature dependent [Ca2+]i spiking is mainly caused by the increased activity of the sarcoendoplasmic reticulum ATPases (SERCAs) that remove Ca2+ from the cytosol into the endoplasmic reticulum. Quantitative comparison of experimental data with multiscale simulations supports the SERCA activity hypothesis. Further analysis of multiscale modeling and traditional rate equations indicates that the experimental observations are a spatial phenomenon where increasing pump strength leads to a decoupling of Ca2+ release sites and subsequently to vanishing [Ca2+]i spikes. |
format | Article |
id | doaj-art-79432d1f1ed74a20bf5c0923a50e05b4 |
institution | Kabale University |
issn | 2090-5904 1687-5443 |
language | English |
publishDate | 2015-01-01 |
publisher | Wiley |
record_format | Article |
series | Neural Plasticity |
spelling | doaj-art-79432d1f1ed74a20bf5c0923a50e05b42025-02-03T06:14:04ZengWileyNeural Plasticity2090-59041687-54432015-01-01201510.1155/2015/683490683490Multiscale Modeling Indicates That Temperature Dependent [Ca2+]i Spiking in Astrocytes Is Quantitatively Consistent with Modulated SERCA ActivityNiko Komin0Mahsa Moein1Mark H. Ellisman2Alexander Skupin3Luxembourg Centre for Systems Biomedicine, University of Luxembourg, 7 Avenue des Hauts-Fourneaux, 4362 Esch-sur-Alzette, LuxembourgLuxembourg Centre for Systems Biomedicine, University of Luxembourg, 7 Avenue des Hauts-Fourneaux, 4362 Esch-sur-Alzette, LuxembourgNational Centre for Microscopy and Imaging Research, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0608, USALuxembourg Centre for Systems Biomedicine, University of Luxembourg, 7 Avenue des Hauts-Fourneaux, 4362 Esch-sur-Alzette, LuxembourgChanges in the cytosolic Ca2+ concentration ([Ca2+]i) are the most predominant active signaling mechanism in astrocytes that can modulate neuronal activity and is assumed to influence neuronal plasticity. Although Ca2+ signaling in astrocytes has been intensively studied in the past, our understanding of the signaling mechanism and its impact on tissue level is still incomplete. Here we revisit our previously published data on the strong temperature dependence of Ca2+ signals in both cultured primary astrocytes and astrocytes in acute brain slices of mice. We apply multiscale modeling to test the hypothesis that the temperature dependent [Ca2+]i spiking is mainly caused by the increased activity of the sarcoendoplasmic reticulum ATPases (SERCAs) that remove Ca2+ from the cytosol into the endoplasmic reticulum. Quantitative comparison of experimental data with multiscale simulations supports the SERCA activity hypothesis. Further analysis of multiscale modeling and traditional rate equations indicates that the experimental observations are a spatial phenomenon where increasing pump strength leads to a decoupling of Ca2+ release sites and subsequently to vanishing [Ca2+]i spikes.http://dx.doi.org/10.1155/2015/683490 |
spellingShingle | Niko Komin Mahsa Moein Mark H. Ellisman Alexander Skupin Multiscale Modeling Indicates That Temperature Dependent [Ca2+]i Spiking in Astrocytes Is Quantitatively Consistent with Modulated SERCA Activity Neural Plasticity |
title | Multiscale Modeling Indicates That Temperature Dependent [Ca2+]i Spiking in Astrocytes Is Quantitatively Consistent with Modulated SERCA Activity |
title_full | Multiscale Modeling Indicates That Temperature Dependent [Ca2+]i Spiking in Astrocytes Is Quantitatively Consistent with Modulated SERCA Activity |
title_fullStr | Multiscale Modeling Indicates That Temperature Dependent [Ca2+]i Spiking in Astrocytes Is Quantitatively Consistent with Modulated SERCA Activity |
title_full_unstemmed | Multiscale Modeling Indicates That Temperature Dependent [Ca2+]i Spiking in Astrocytes Is Quantitatively Consistent with Modulated SERCA Activity |
title_short | Multiscale Modeling Indicates That Temperature Dependent [Ca2+]i Spiking in Astrocytes Is Quantitatively Consistent with Modulated SERCA Activity |
title_sort | multiscale modeling indicates that temperature dependent ca2 i spiking in astrocytes is quantitatively consistent with modulated serca activity |
url | http://dx.doi.org/10.1155/2015/683490 |
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