The interplay of intracellular calcium and zinc ions in response to electric field stimulation in primary rat cortical neurons in vitro
Recent pharmacological studies demonstrate a role for zinc (Zn2+) in shaping intracellular calcium (Ca2+) dynamics and vice versa in excitable cells including neurons and cardiomyocytes. Herein, we sought to examine the dynamic of intracellular release of Ca2+ and Zn2+ upon modifying excitability of...
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Frontiers Media S.A.
2023-04-01
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Series: | Frontiers in Cellular Neuroscience |
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Online Access: | https://www.frontiersin.org/articles/10.3389/fncel.2023.1118335/full |
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author | Abdullah J. Alshawaf Abdullah J. Alshawaf Sarah A. Alnassar Futwan A. Al-Mohanna |
author_facet | Abdullah J. Alshawaf Abdullah J. Alshawaf Sarah A. Alnassar Futwan A. Al-Mohanna |
author_sort | Abdullah J. Alshawaf |
collection | DOAJ |
description | Recent pharmacological studies demonstrate a role for zinc (Zn2+) in shaping intracellular calcium (Ca2+) dynamics and vice versa in excitable cells including neurons and cardiomyocytes. Herein, we sought to examine the dynamic of intracellular release of Ca2+ and Zn2+ upon modifying excitability of primary rat cortical neurons using electric field stimulation (EFS) in vitro. We show that exposure to EFS with an intensity of 7.69 V/cm induces transient membrane hyperpolarization together with transient elevations in the cytosolic levels of Ca2+ and Zn2+ ions. The EFS-induced hyperpolarization was inhibited by prior treatment of cells with the K+ channel opener diazoxide. Chemical hyperpolarization had no apparent effect on either Ca2+ or Zn2+. The source of EFS-induced rise in Ca2+ and Zn2+ seemed to be intracellular, and that the dynamic inferred of an interplay between Ca2+ and Zn2+ ions, whereby the removal of extracellular Ca2+ augmented the release of intracellular Ca2+ and Zn2+ and caused a stronger and more sustained hyperpolarization. We demonstrate that Zn2+ is released from intracellular vesicles located in the soma, with major co-localizations in the lysosomes and endoplasmic reticulum. These studies further support the use of EFS as a tool to interrogate the kinetics of intracellular ions in response to changing membrane potential in vitro. |
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language | English |
last_indexed | 2024-04-09T15:45:12Z |
publishDate | 2023-04-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Cellular Neuroscience |
spelling | doaj.art-60699c021fb743d48bc75ed99b788a6c2023-04-27T04:30:26ZengFrontiers Media S.A.Frontiers in Cellular Neuroscience1662-51022023-04-011710.3389/fncel.2023.11183351118335The interplay of intracellular calcium and zinc ions in response to electric field stimulation in primary rat cortical neurons in vitroAbdullah J. Alshawaf0Abdullah J. Alshawaf1Sarah A. Alnassar2Futwan A. Al-Mohanna3Department of Physiological Sciences, College of Medicine, Alfaisal University, Riyadh, Saudi ArabiaDepartment of Cell Biology, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi ArabiaDepartment of Cell Biology, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi ArabiaDepartment of Cell Biology, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi ArabiaRecent pharmacological studies demonstrate a role for zinc (Zn2+) in shaping intracellular calcium (Ca2+) dynamics and vice versa in excitable cells including neurons and cardiomyocytes. Herein, we sought to examine the dynamic of intracellular release of Ca2+ and Zn2+ upon modifying excitability of primary rat cortical neurons using electric field stimulation (EFS) in vitro. We show that exposure to EFS with an intensity of 7.69 V/cm induces transient membrane hyperpolarization together with transient elevations in the cytosolic levels of Ca2+ and Zn2+ ions. The EFS-induced hyperpolarization was inhibited by prior treatment of cells with the K+ channel opener diazoxide. Chemical hyperpolarization had no apparent effect on either Ca2+ or Zn2+. The source of EFS-induced rise in Ca2+ and Zn2+ seemed to be intracellular, and that the dynamic inferred of an interplay between Ca2+ and Zn2+ ions, whereby the removal of extracellular Ca2+ augmented the release of intracellular Ca2+ and Zn2+ and caused a stronger and more sustained hyperpolarization. We demonstrate that Zn2+ is released from intracellular vesicles located in the soma, with major co-localizations in the lysosomes and endoplasmic reticulum. These studies further support the use of EFS as a tool to interrogate the kinetics of intracellular ions in response to changing membrane potential in vitro.https://www.frontiersin.org/articles/10.3389/fncel.2023.1118335/fullelectric field stimulationcalciumzincmembrane potentialcortical neurons |
spellingShingle | Abdullah J. Alshawaf Abdullah J. Alshawaf Sarah A. Alnassar Futwan A. Al-Mohanna The interplay of intracellular calcium and zinc ions in response to electric field stimulation in primary rat cortical neurons in vitro Frontiers in Cellular Neuroscience electric field stimulation calcium zinc membrane potential cortical neurons |
title | The interplay of intracellular calcium and zinc ions in response to electric field stimulation in primary rat cortical neurons in vitro |
title_full | The interplay of intracellular calcium and zinc ions in response to electric field stimulation in primary rat cortical neurons in vitro |
title_fullStr | The interplay of intracellular calcium and zinc ions in response to electric field stimulation in primary rat cortical neurons in vitro |
title_full_unstemmed | The interplay of intracellular calcium and zinc ions in response to electric field stimulation in primary rat cortical neurons in vitro |
title_short | The interplay of intracellular calcium and zinc ions in response to electric field stimulation in primary rat cortical neurons in vitro |
title_sort | interplay of intracellular calcium and zinc ions in response to electric field stimulation in primary rat cortical neurons in vitro |
topic | electric field stimulation calcium zinc membrane potential cortical neurons |
url | https://www.frontiersin.org/articles/10.3389/fncel.2023.1118335/full |
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