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Store-operated calcium entry is essential for glial calcium signalling in CNS white matter

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Store-operated calcium entry is essential for glial calcium signalling in CNS white matter. / Papanikolaou, M.; Lewis, A.; Butt, A. M.

In: Brain Structure & Function, 28.02.2017.

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Papanikolaou, M.; Lewis, A.; Butt, A. M. / Store-operated calcium entry is essential for glial calcium signalling in CNS white matter.

In: Brain Structure & Function, 28.02.2017.

Research output: Contribution to journalArticle

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@article{ce38b46358744035a768f30cd74a26fa,
title = "Store-operated calcium entry is essential for glial calcium signalling in CNS white matter",
abstract = "‘Calcium signalling’ is the ubiquitous response of glial cells to multiple extracellular stimuli. The primary mechanism of glial calcium signalling is by release of calcium from intracellular stores of the endoplasmic reticulum (ER). Replenishment of ER Ca2+ stores relies on store-operated calcium entry (SOCE). However, despite the importance of calcium signalling in glial cells, little is known about their mechanisms of SOCE. Here, we investigated SOCE in glia of the mouse optic nerve, a typical CNS white matter tract that comprises bundles of myelinated axons and the oligodendrocytes and astrocytes that support them. Using quantitative RT-PCR, we identified Orai1 channels, both Stim1 and Stim2, and the transient receptor potential M3 channel (TRPM3) as the primary channels for SOCE in the optic nerve, and their expression in both astrocytes and oligodendrocytes was demonstrated by immunolabelling of optic nerve sections and cultures. The functional importance of SOCE was demonstrated by fluo-4 calcium imaging on isolated intact optic nerves and optic nerve cultures. Removal of extracellular calcium ([Ca2+]o) resulted in a marked depletion of glial cytosolic calcium ([Ca2+]i), which recovered rapidly on restoration of [Ca2+]o via SOCE. 2-aminoethoxydiphenylborane (2APB) significantly decreased SOCE and severely attenuated ATP-mediated calcium signalling. The results provide evidence that Orai/Stim and TRPM3 are important components of the ‘calcium toolkit’ that underpins SOCE and the sustainability of calcium signalling in white matter glia.",
keywords = "Store-operated calcium channel, CRAC, TRP channel, Glia, Astrocyte, Oligodendrocyte, White matter, Calcium signalling, RCUK, BBSRC, BB/J016888",
author = "M. Papanikolaou and A. Lewis and Butt, {A. M.}",
year = "2017",
month = "2",
doi = "10.1007/s00429-017-1380-8",
journal = "Brain Structure & Function",
issn = "1863-2653",
publisher = "Springer Verlag",

}

RIS

TY - JOUR

T1 - Store-operated calcium entry is essential for glial calcium signalling in CNS white matter

AU - Papanikolaou,M.

AU - Lewis,A.

AU - Butt,A. M.

PY - 2017/2/28

Y1 - 2017/2/28

N2 - ‘Calcium signalling’ is the ubiquitous response of glial cells to multiple extracellular stimuli. The primary mechanism of glial calcium signalling is by release of calcium from intracellular stores of the endoplasmic reticulum (ER). Replenishment of ER Ca2+ stores relies on store-operated calcium entry (SOCE). However, despite the importance of calcium signalling in glial cells, little is known about their mechanisms of SOCE. Here, we investigated SOCE in glia of the mouse optic nerve, a typical CNS white matter tract that comprises bundles of myelinated axons and the oligodendrocytes and astrocytes that support them. Using quantitative RT-PCR, we identified Orai1 channels, both Stim1 and Stim2, and the transient receptor potential M3 channel (TRPM3) as the primary channels for SOCE in the optic nerve, and their expression in both astrocytes and oligodendrocytes was demonstrated by immunolabelling of optic nerve sections and cultures. The functional importance of SOCE was demonstrated by fluo-4 calcium imaging on isolated intact optic nerves and optic nerve cultures. Removal of extracellular calcium ([Ca2+]o) resulted in a marked depletion of glial cytosolic calcium ([Ca2+]i), which recovered rapidly on restoration of [Ca2+]o via SOCE. 2-aminoethoxydiphenylborane (2APB) significantly decreased SOCE and severely attenuated ATP-mediated calcium signalling. The results provide evidence that Orai/Stim and TRPM3 are important components of the ‘calcium toolkit’ that underpins SOCE and the sustainability of calcium signalling in white matter glia.

AB - ‘Calcium signalling’ is the ubiquitous response of glial cells to multiple extracellular stimuli. The primary mechanism of glial calcium signalling is by release of calcium from intracellular stores of the endoplasmic reticulum (ER). Replenishment of ER Ca2+ stores relies on store-operated calcium entry (SOCE). However, despite the importance of calcium signalling in glial cells, little is known about their mechanisms of SOCE. Here, we investigated SOCE in glia of the mouse optic nerve, a typical CNS white matter tract that comprises bundles of myelinated axons and the oligodendrocytes and astrocytes that support them. Using quantitative RT-PCR, we identified Orai1 channels, both Stim1 and Stim2, and the transient receptor potential M3 channel (TRPM3) as the primary channels for SOCE in the optic nerve, and their expression in both astrocytes and oligodendrocytes was demonstrated by immunolabelling of optic nerve sections and cultures. The functional importance of SOCE was demonstrated by fluo-4 calcium imaging on isolated intact optic nerves and optic nerve cultures. Removal of extracellular calcium ([Ca2+]o) resulted in a marked depletion of glial cytosolic calcium ([Ca2+]i), which recovered rapidly on restoration of [Ca2+]o via SOCE. 2-aminoethoxydiphenylborane (2APB) significantly decreased SOCE and severely attenuated ATP-mediated calcium signalling. The results provide evidence that Orai/Stim and TRPM3 are important components of the ‘calcium toolkit’ that underpins SOCE and the sustainability of calcium signalling in white matter glia.

KW - Store-operated calcium channel

KW - CRAC

KW - TRP channel

KW - Glia

KW - Astrocyte

KW - Oligodendrocyte

KW - White matter

KW - Calcium signalling

KW - RCUK

KW - BBSRC

KW - BB/J016888

U2 - 10.1007/s00429-017-1380-8

DO - 10.1007/s00429-017-1380-8

M3 - Article

JO - Brain Structure & Function

T2 - Brain Structure & Function

JF - Brain Structure & Function

SN - 1863-2653

ER -

ID: 6842108