SOCE in neurons: Signaling or just refilling?

Majewski, Łukasz; Kuźnicki, Jacek

doi:10.1016/j.bbamcr.2015.01.019

Cited by 85 publications

(90 citation statements)

References 230 publications

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“…STIMs can also induce Ca 2+ influx via transient receptor potential (TRP) channels (Salido et al, 2011; Hartmann et al, 2014; Shin et al, 2016). Ca 2+ that enters the cell is then transported to the ER through activity of the sarcoplasmic reticulum Ca 2+ -adenosine triphosphatase (SERCA) pump to refill ER stores and can be used for signaling (for review see Majewski and Kuznicki, 2015). In contrast to non-excitable cells, Ca 2+ entry into neurons can occur via additional pathways.…”

Section: Introductionmentioning

confidence: 99%

AMPA Receptors Are Involved in Store-Operated Calcium Entry and Interact with STIM Proteins in Rat Primary Cortical Neurons

Gruszczynska-Biegala

Sladowska

Kuźnicki

2016

Front. Cell. Neurosci.

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The process of store-operated calcium entry (SOCE) leads to refilling the endoplasmic reticulum (ER) with calcium ions (Ca2+) after their release into the cytoplasm. Interactions between (ER)-located Ca2+ sensors (stromal interaction molecule 1 [STIM1] and STIM2) and plasma membrane-located Ca2+ channel-forming protein (Orai1) underlie SOCE and are well described in non-excitable cells. In neurons, however, SOCE appears to be more complex because of the importance of Ca2+ influx via voltage-gated or ionotropic receptor-operated Ca2+ channels. We found that the SOCE inhibitors ML-9 and SKF96365 reduced α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-induced [Ca2+]i amplitude by 80% and 53%, respectively. To assess the possible involvement of AMPA receptors (AMPARs) in SOCE, we used their specific inhibitors. As estimated by Fura-2 acetoxymethyl (AM) single-cell Ca2+ measurements in the presence of CNQX or NBQX, thapsigargin (TG)-induced Ca2+ influx decreased 2.2 or 3.7 times, respectively. These results suggest that under experimental conditions of SOCE when Ca2+ stores are depleted, Ca2+ can enter neurons also through AMPARs. Using specific antibodies against STIM proteins or GluA1/GluA2 AMPAR subunits, co-immunoprecipitation assays indicated that when Ca2+ levels are low in the neuronal ER, a physical association occurs between endogenous STIM proteins and endogenous AMPAR receptors. Altogether, our data suggest that STIM proteins in neurons can control AMPA-induced Ca2+ entry as a part of the mechanism of SOCE.

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Section: Introductionmentioning

confidence: 99%

AMPA Receptors Are Involved in Store-Operated Calcium Entry and Interact with STIM Proteins in Rat Primary Cortical Neurons

Gruszczynska-Biegala

Sladowska

Kuźnicki

2016

Front. Cell. Neurosci.

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“…A process linking these two mechanisms is store-operated Ca 2+ entry (SOCE), whereby the depletion of ER Ca 2+ store activates the opening of plasma membrane Ca 2+ channels [40]. SOCE was originally thought to provide direct Ca 2+ signals to recipients localized to spatially restricted areas close to the sites of Ca 2+ entry to initiate specific signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

FAM3A Protects Against Glutamate-Induced Toxicity by Preserving Calcium Homeostasis in Differentiated PC12 Cells

Song

Gou

Zou

2017

Cell Physiol Biochem

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Background/Aims: Stroke is the leading cause of adult disability, and glutamate-induced dysregulation of intracellular Ca²⁺ homeostasis is a key mechanism. FAM3A is the first member of the family with sequence similarity 3 (FAM3) gene family, and its biological function remains largely unknown. We have recently reported that FAM3A exerts protective effects against oxidative stress and mitochondrial dysfunction in HT22 cells. Methods: Here, we investigated the protective effects of FAM3A using a glutamate-induced neuronal injury model in nerve growth factor (NGF)-differentiated PC12 cells. The protective effects were determined by measuring lactate dehydrogenase (LDH) release, apoptosis and mitochondrial oxidative stress. Ca²⁺ imaging was performed to detect changes in intracellular Ca²⁺ concentration in PC12 cells. The related molecular mechanisms were investigated by fluorescence staining, coimmunoprecipitation (Co-IP) and western blotting. Results: Upregulation of FAM3A by lentivirus transfection markedly decreased LDH release, inhibited apoptosis and reduced mitochondrial oxidative stress, which were accompanied by alleviated intracellular Ca²⁺ levels as measured by calcium imaging. The results of western blotting showed that FAM3A significantly decreased the surface expression of metabotropic glutamate receptor 1/5 (mGluR1/5), with no effect on the expression of N-methyl-d-aspartic acid receptor (NMDAR) or α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor (AMPAR) subunits. FAM3A overexpression also inhibited the intracellular Ca²⁺ release mediated by mGluR1/5 and inositol 1,4,5-trisphosphate receptor (IP₃R), but not the ryanodine receptor (RyR). In addition, FAM3A significantly attenuated the store-operated calcium entry (SOCE) induced by thapsigargin (Tg), but the expression of SOCE-related proteins was not altered. The results of coimmunoprecipitation (Co-IP) showed that FAM3A disrupted the interaction of stromal interaction molecule 1 (STIM1) with Orai1 triggered by glutamate. Conclusion: These results suggest that the upregulation of FAM3A protects against glutamate-induced dysfunction of Ca²⁺ homeostasis not only by inhibiting mGluR1/5-dependent endoplasmic reticulum (ER) Ca²⁺ release, but also by attenuating SOCE mediated by the STIM1-Orai1 interaction.

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“…Specifically, there are strong lines of evidence that the induction of bidirectional synaptic plasticity in the hippocampus is mediated by different calcium sources, with certain protocols requiring synergistic activation of multiple calcium 16, 2017; sources (Brager and Johnston, 2007;Christie et al, 1996;Golding et al, 2002;Huber et al, 1995;Nishiyama et al, 2000;Raymond, 2007). These studies show that plasticity induction is dependent on influx of calcium through NMDA receptors (Christie et al, 1996;Collingridge and Bliss, 1987;Collingridge et al, 1983;Morris et al, 1986;Mulkey and Malenka, 1992;Nishiyama et al, 2000;Tsien et al, 1996;Wang et al, 2003), voltage-gated calcium channels (Brager and Johnston, 2007;Christie et al, 1996;Christie et al, 1997;Johnston et al, 1992;Moosmang et al, 2005;Nicholson and Kullmann, 2017;Wang et al, 2003), store-operated calcium channels (Baba et al, 2003;Garcia-Alvarez et al, 2015;Majewski and Kuznicki, 2015;Majewski et al, 2016;Prakriya and Lewis, 2015) and receptors on the ER activated by metabotropic receptors on the plasma membrane (Huber et al, 2000;Nishiyama et al, 2000;Verkhratsky, 2002). Additionally, voltage-gated channels and their auxiliary subunits (Anirudhan and Narayanan, 2015;Brager et al, 2013;Chen et al, 2006;Chung et al, 2009a;Chung et al, 2009b;Johnston et al,...…”

Section: Degeneracy In Calcium Regulation and In The Induction Of Synmentioning

confidence: 99%

Degeneracy in hippocampal physiology and plasticity

Rathour

Narayanan

2017

Preprint

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Degeneracy, defined as the ability of structurally disparate elements to perform analogous function, has largely been assessed from the perspective of maintaining robustness of physiology or plasticity. How does the framework of degeneracy assimilate into an encoding system where the ability to change is an essential ingredient for storing new incoming information? Could degeneracy maintain the balance between the apparently contradictory goals of the need to change for encoding and the need to resist change towards maintaining homeostasis? In this review, we explore these fundamental questions with the mammalian hippocampus as an example encoding system. We systematically catalog lines of evidence, spanning multiple scales of analysis, that demonstrate the expression of degeneracy in hippocampal physiology and plasticity. We assess the potential of degeneracy as a framework to achieve encoding and homeostasis without cross-interferences, and postulate that multiscale parametric and interactional complexity could establish disparate routes towards accomplishing these conjoint goals. These disparate routes then provide several degrees of freedom to the encodinghomeostasis system in accomplishing its tasks in an input-and state-dependent manner. Finally, the expression of degeneracy spanning multiple scales offers an ideal reconciliation to several outstanding controversies, through the recognition that the seemingly contradictory disparate observations are merely alternate routes that the system might recruit towards accomplishment of its goals. Juxtaposed against the ubiquitous prevalence of degeneracy and its strong links to evolution, it is perhaps apt to add a corollary to Theodosius Dobzhansky's famous quote and state "nothing in physiology makes sense except in the light of degeneracy".peer-reviewed)

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SOCE in neurons: Signaling or just refilling?

Cited by 85 publications

References 230 publications

AMPA Receptors Are Involved in Store-Operated Calcium Entry and Interact with STIM Proteins in Rat Primary Cortical Neurons

AMPA Receptors Are Involved in Store-Operated Calcium Entry and Interact with STIM Proteins in Rat Primary Cortical Neurons

FAM3A Protects Against Glutamate-Induced Toxicity by Preserving Calcium Homeostasis in Differentiated PC12 Cells

Degeneracy in hippocampal physiology and plasticity

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