Expression of STIM1 in brain and puncta-like co-localization of STIM1 and ORAI1 upon depletion of Ca2+ store in neurons

Klejman, Monika E.; Gruszczynska-Biegala, Joanna; Skibinska-Kijek, Anna; Wisniewska, M.; Misztal, Katarzyna; Błażejczyk, Magdalena; Bojarski, Łukasz; Kuźnicki, Jacek

doi:10.1016/j.neuint.2008.10.005

Cited by 88 publications

(102 citation statements)

References 40 publications

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“…Here we found that also I BMAA is due to activation of TRPC-like channels, through mGluR1. This conclusion is supported by the following evidence: (1) I BMAA was reduced by the nonselective TRPC channels blockers SKF 96365 and RR; (2) the I BMAA reversal potential was ϳ0 mV, consistent with the activation of a TRPC-mediated mixed cation current (Okada et al, 1998;Strubing et al, 2001;Tozzi et al, 2003); (3) Orai1 and STIM1, proteins that are likely to interact with TRPC channels downstream of G-protein-coupled receptor activation (Wang et al, 2008;Kim et al, 2009;Klejman et al, 2009;Liao et al, 2009) (for review, see Cahalan, 2009), were expressed in biocytinloaded neurons; (4) CPCCOEt and SKF 96365 did not have additive effects on I BMAA , demonstrating that mGluR1 activation and TRPC-like channel opening are two subsequent steps in the BMAA-induced pathway. Interestingly, GABAergic SNpc cells responded to BMAA with an AMPA-mediated inward current that was not associated with an intracellular calcium increase.…”

Section: Discussionmentioning

confidence: 80%

Metabotropic Glutamate Receptor 1 Mediates the Electrophysiological and Toxic Actions of the Cycad Derivative β-N-Methylamino-l-Alanine on Substantia Nigra Pars Compacta DAergic Neurons

et al. 2010

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Amyotrophic lateral sclerosis-Parkinson dementia complex (ALS-PDC) is a neurodegenerative disease with ALS, parkinsonism, andAlzheimer's symptoms that is prevalent in the Guam population. ␤-N-Methylamino alanine (BMAA) has been proposed as the toxic agent damaging several neuronal types in ALS-PDC, including substantia nigra pars compacta dopaminergic (SNpc DAergic) neurons. BMAA is a mixed glutamate receptor agonist, but the specific pathways activated in DAergic neurons are not yet known. We combined electrophysiology, microfluorometry, and confocal microscopy analysis to monitor membrane potential/current, cytosolic calcium concentration (

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Section: Discussionmentioning

confidence: 80%

Metabotropic Glutamate Receptor 1 Mediates the Electrophysiological and Toxic Actions of the Cycad Derivative β-N-Methylamino-l-Alanine on Substantia Nigra Pars Compacta DAergic Neurons

et al. 2010

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“…When ER stores are depleted, the ER-resident stromal interaction molecule 1 (STIM1) localizes to the ER and plasma membrane junctions [31][32][33]. From here, STIM1 facilitates SOCE [34] through store-operated calcium (SOC) channels which utilize transient receptor potential cation (TRPC) channels and ORAI1, and calcium release-activated calcium (CRAC) channels which depend primarily on ORAI1 [33,[35][36][37].…”

Section: Glossarymentioning

confidence: 98%

Calcium signaling in axon guidance

Sutherland

Pujic

Goodhill

2014

Trends in Neurosciences

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“…The absence of diffuse neuronal FM dye labeling is surprising given that SOCE, Orai1, STIM1, and TRPC1 are expressed by neurons (57). One reason might be a different channel density, because in neurons Ca 2ϩ influx is mostly caused by voltage-gated Ca 2ϩ channels, whereas the astroglial Ca 2ϩ signaling is dominated by SOCE and relies on the near-membrane ER to rapidly replenish the ER stores (2).…”

Section: Permeant Fm Dyes Facilitate Er Store Depletion and Fm Dye Enmentioning

confidence: 99%

FM dyes enter via a store-operated calcium channel and modify calcium signaling of cultured astrocytes

Hérault

Oheim

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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The amphiphilic fluorescent styryl pyridinium dyes FM1-43 and FM4-64 are used to probe activity-dependent synaptic vesicle cycling in neurons. Cultured astrocytes can internalize FM1-43 and FM4-64 inside vesicles but their uptake is insensitive to the elevation of cytosolic calcium (Ca 2؉ ) concentration and the underlying mechanism remains unclear. Here we used total internal reflection fluorescence microscopy and pharmacological tools to study the mechanisms of FM4-64 uptake into cultured astrocytes from mouse neocortex. Our data show that: (i) endocytosis is not a major route for FM4-64 uptake into astrocytes; (ii) FM4-64 enters astrocytes through an aqueous pore and strongly affects Ca 2؉ homeostasis; (iii) partitioning of FM4-64 into the outer leaflet of the plasma membrane results in a facilitation of store-operated Ca 2؉ entry (SOCE) channel gating; (iv) FM4-64 permeates and competes with Ca 2؉ for entry through a SOCE channel; (v) intracellular FM4-64 mobilizes Ca 2؉ from the endoplasmic reticulum stores, conveying a positive feedback to activate SOCE and to sustain dye uptake into astrocytes. Our study demonstrates that FM dyes are not markers of cycling vesicles in astrocytes and calls for a careful interpretation of FM fluorescence.calcium homeostasis ͉ endoplasmic reticulum ͉ lipid bilayer ͉ styryl dye ͉ TIRF I n astrocytes the strong expression of the plasma membrane (PM) store-operated Ca 2ϩ entry (SOCE) (1-4) contrasts with a relatively small expression of voltage-gated channels and AMPA/ NMDA ligand-gated channels that are mostly expressed by neurons. In response to neuronal activity and neurotransmitter release, the activation of astroglial metabotropic receptors induces a reduction of the endoplasmic reticulum (ER) Ca 2ϩ concentration ([Ca 2ϩ ] ER ) that leads to the activation of the SOCE and to an elevation of the intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) (4) that is critical for the electrically silent astrocytes to release gliotransmitters and control nearby neurons, glia, and blood vessels (5). The type 1-2 stromal interaction molecules (STIM1-2) and Orai1-3 membrane proteins are key components of the SOCE, being the ER Ca 2ϩ sensor and the PM pore-forming subunit, respectively (6, 7). A possible participation of the classical transient receptor potential (TRPC) channels to the protein complex generating the SOCE is debated in several cell types (8), including astrocytes (3).Styryl pyridinium FM dyes are amphiphilic molecules that reversibly partition in lipid membranes. Their positively charged pyridinium head prevents them from diffusing through the PM. Only weakly fluorescent in aqueous solution their quantum yield increases in a lipid environment. Their activity-dependent uptake and destaining has made them common probes for synaptic vesicle cycling at the nerve terminals (9-11). Cultured astrocytes internalize FM dyes (3,(12)(13)(14)(15)(16)(17)(18). However, this uptake is not modified by the activation of metabotropic glutamate receptors (19), and its mechanism remains elusiv...

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Expression of STIM1 in brain and puncta-like co-localization of STIM1 and ORAI1 upon depletion of Ca2+ store in neurons

Cited by 88 publications

References 40 publications

Metabotropic Glutamate Receptor 1 Mediates the Electrophysiological and Toxic Actions of the Cycad Derivative β-N-Methylamino-l-Alanine on Substantia Nigra Pars Compacta DAergic Neurons

Metabotropic Glutamate Receptor 1 Mediates the Electrophysiological and Toxic Actions of the Cycad Derivative β-N-Methylamino-l-Alanine on Substantia Nigra Pars Compacta DAergic Neurons

Calcium signaling in axon guidance

FM dyes enter via a store-operated calcium channel and modify calcium signaling of cultured astrocytes

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