Store-operated calcium entry compensates fast ER calcium loss in resting hippocampal neurons

Samtleben, Samira; Wachter, Britta; Blum, Robert

doi:10.1016/j.ceca.2015.04.002

Cited by 32 publications

(51 citation statements)

References 71 publications

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“…Figure 1D), as now documented by several groups in different types of neurons [4][5][6][7][8]. In fact, depletion of ER and cytoplasmic Ca 2+ is so fast that it partially occludes or masks thapsigargin-mediated ER Ca 2+ release ( Figure 1C).…”

Section: Soce Refers To a Unique Casupporting

confidence: 70%

Neuronal SOCE: Myth or Reality?

Lü

Fivaz

2016

Trends in Cell Biology

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Section: Soce Refers To a Unique Casupporting

confidence: 70%

Neuronal SOCE: Myth or Reality?

Lü

Fivaz

2016

Trends in Cell Biology

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“…Gas phase concentrations in the incubator were verified by infrared absorbance of the effluent gas, and were constantly monitored and maintained at the appropriate concentrations throughout the experiments using an infrared Ohmeda 5330 Agent Monitor (Datex-Ohmeda; GE Healthcare Life Sciences, Pittsburgh, PA, USA). Since the experimental cell culture plates were inside the sealed anesthetic exposure chamber, which was continuously perfused with a constant concentration of anesthetic, the anesthetic concentration in the cell culture medium remained stable as previously reported (11). There was no evidence of anesthetic degradation in the cell culture over an 8 h time period.…”

Section: Methodsmentioning

confidence: 90%

“…In response to stress, neurons will instantly improve [Ca 2+ ] c levels, in order to trigger a series of physiological activities. The ER is the primary source of releasable intracellular calcium in neurons (11) and has an important role in the maintenance of intracellular calcium homeostasis, protein synthesis, cell survival and apoptosis (14,15). RyR and IP3R are calcium-activated calcium release channels that are present on the ER membrane.…”

Section: Discussionmentioning

confidence: 99%

“…Our previously published and current data suggested that overactivation of IP3R may contribute to isoflurane-induced calcium elevation and cell apoptosis. Excessive calcium release from the ER via IP3R may induce calcium overload in the mitochondria and depletion of ER calcium (11), which may result in collapse of the mitochondrial membrane potential and promotion of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

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A mutation in β-amyloid precursor protein renders SH-SY5Y cells vulnerable to isoflurane toxicity: The role of inositol 1,4,5-trisphosphate receptors

Liu

Song

Wang

et al. 2016

Molecular Medicine Reports

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Isoflurane is a commonly used inhaled anesthetic, which induces apoptosis of SH-SY5Y cells in a dose- and time-dependent manner; however, the underlying mechanisms remain unknown. The authors of the present study hypothesized that a mutation in β-amyloid precursor protein (APP), which is a gene associated with familial Alzheimer's disease, may render cells vulnerable to isoflurane-induced cytotoxicity via activation of inositol 1,4,5-trisphosphate receptors (IP3R). In the present study, SH-SY5Y cells were transfected with a vector or with mutated APP, and were treated with the equivalent of 1 minimum alveolar concentration (MAC) isoflurane for 8 h. Cell apoptosis rate, alterations to cytosolic calcium concentrations ([Ca2+]c), and protein levels of IP3R were determined following exposure of cells to isoflurane. In addition, the effects of the IP3R antagonist xestospongin C were determined on isoflurane-induced cytotoxicity and calcium release from the endoplasmic reticulum (ER) of mutated APP- and vector-transfected SH-SY5Y cells. Treatment with isoflurane (1 MAC) for 8 h induced a higher degree of cytotoxicity, and a marked increase in [Ca2+]c and IP3R protein levels in mutated APP-transfected SH-SY5Y cells compared with vector-transfected SH-SY5Y cells. Xestospongin C significantly attenuated isoflurane-mediated cytotoxicity and inhibited calcium release from the ER of SH-SY5Y cells. These results indicated that the APP mutation may render SH-SY5Y cells vulnerable to isoflurane neurotoxicity, and the underlying mechanism may be associated with Ca2+ dysregulation via overactivation of IP3R.

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“…Conversely, the relevance of neuronal SOCE is being debated (Lu and Fivaz, 2016 ). In the last few years, SOCE activity has been observed in hippocampal (Emptage et al, 2001 ; Baba et al, 2003 ; Kann et al, 2012 ; Sun et al, 2014 ; Samtleben et al, 2015 ), cortical (Berna-Erro et al, 2009 ; Klejman et al, 2009 ; Gruszczynska-Biegala et al, 2011 ), cerebellar (Baba et al, 2003 ; Hartmann et al, 2014 ), sensory (Gemes et al, 2011 ) and dorsal horn neurons (Xia et al, 2014 ). Moreover, two independent groups found that STIM1 directly modulates depolarization-induced opening of the voltage-gated Ca 2+ channel Ca V 1.2 (Park et al, 2010 ; Wang et al, 2010 ).…”

Section: Introductionmentioning

confidence: 99%

Store-Operated Calcium Entry Is Required for mGluR-Dependent Long Term Depression in Cortical Neurons

González-Sánchez

Arco

Esteban

et al. 2017

Front. Cell. Neurosci.

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Store-operated calcium entry (SOCE) is a Calcium (Ca2+) influx pathway activated by depletion of intracellular stores that occurs in eukaryotic cells. In neurons, the presence and functions of SOCE are still in question. Here, we show evidences for the existence of SOCE in primary mouse cortical neurons. Endoplasmic reticulum (ER)-Ca2+ depletion using thapsigargin (Tg) triggered a maintained cytosolic Ca2+ increase, which rapidly returned to basal level in the presence of the SOCE blockers 2-Aminoethoxydiphenyl borate (2-APB) and YM-58483. Neural SOCE is also engaged by activation of metabotropic glutamate receptors (mGluRs) with (S)-3,5-dihydroxyphenylglycine (DHPG) (agonist of group I mGluRs), being an essential mechanism to maintain the mGluR-driven Ca2+ signal. Activation of group I of mGluRs triggers long-term depression (LTD) in many brain regions, but the underlying mechanism and, specifically, the necessity of Ca2+ increase in the postsynaptic neuron is controversial. In primary cortical neurons, we now show that the inhibition of Ca2+ influx through SOCE impaired DHPG-LTD, pointing out a key function of calcium and SOCE in synaptic plasticity.

show abstract

Store-operated calcium entry compensates fast ER calcium loss in resting hippocampal neurons

Cited by 32 publications

References 71 publications

Neuronal SOCE: Myth or Reality?

Neuronal SOCE: Myth or Reality?

A mutation in β-amyloid precursor protein renders SH-SY5Y cells vulnerable to isoflurane toxicity: The role of inositol 1,4,5-trisphosphate receptors

Store-Operated Calcium Entry Is Required for mGluR-Dependent Long Term Depression in Cortical Neurons

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