Store-operated calcium entry modulates neuronal network activity in a model of chronic epilepsy

Steinbeck, Julius A.; Henke, Nadine; Opatz, Jessica; Gruszczynska-Biegala, Joanna; Schneider, Lars; Theiss, Stephan; Hamacher, Nadine; Steinfarz, Barbara; Gölz, Stefan; Brüstle, Oliver; Kuźnicki, Jacek; Methner, Axel

doi:10.1016/j.expneurol.2011.08.022

Cited by 70 publications

(71 citation statements)

References 36 publications

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“…From this evidence, it was proposed that STIM2 -/-mice are protected from ischemic stroke. In contrast to the findings of Berna-Erro, several other groups have detected neuronal STIM1 expression [127][128][129] . However, the precise contribution of STIM1 to neuronal function remains to be elucidated.…”

Section: +contrasting

confidence: 76%

Loss of endoplasmic reticulum Ca2+ homeostasis: contribution to neuronal cell death during cerebral ischemia

Bodalia

Jackson

2012

Acta Pharmacol Sin

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The loss of Ca 2+ homeostasis during cerebral ischemia is a hallmark of impending neuronal demise. Accordingly, considerable cellular resources are expended in maintaining low resting cytosolic levels of Ca 2+ . These include contributions by a host of proteins involved in the sequestration and transport of Ca 2+ , many of which are expressed within intracellular organelles, including lysosomes, mitochondria as well as the endoplasmic reticulum (ER homeostasis is an important trigger of pathological processes. Here we review a growing body of evidence suggesting that ER dysfunction is an important factor contributing to neuronal injury and loss post-ischemia. Specifically, the contribution of the ER to cytosolic Ca 2+ elevations during ischemia will be considered, as will the signalling cascades recruited as a consequence of disrupting ER homeostasis and function.

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Section: +contrasting

confidence: 76%

Loss of endoplasmic reticulum Ca2+ homeostasis: contribution to neuronal cell death during cerebral ischemia

Bodalia

Jackson

2012

Acta Pharmacol Sin

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“…has been demonstrated to contribute to the regulation of neural differentiation of ESCs as well as play a role in a variety of other neuronal activities. These include regulating the firing of the flight motor neurons in Drosophila melanogaster [78]; modulating the activity of the neuronal network in chronic epilepsy [79]; and regulating neuronal excitability, especially in injured neurons [80]. In addition, knockdown of STIM1 not only inhibited the differentiation of mouse Sox1-GFP 46C ESCs into neural progenitors, neurons and astrocytes but also caused severe cell death and suppresses the proliferation of neural progenitors during the early stage of neural differentiation [22].…”

Section: The Expression Of Ca 2+ -Binding Proteins During Neural Diffmentioning

confidence: 99%

The role of Ca2+ signaling on the self-renewal and neural differentiation of embryonic stem cells (ESCs)

et al. 2016

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Embryonic stem cells (ESCs) are promising resources for both scientific research and clinical regenerative medicine. With regards to the latter, ESCs are especially useful for treating several neurodegenerative disorders. Two significant characteristics of ESCs, which make them so valuable, are their capacity for self-renewal and their pluripotency, both of which are regulated by the integration of various signaling pathways. Intracellular Ca 2+ signaling is involved in several of these pathways. It is known to be precisely controlled by different Ca 2+ channels and pumps, which play an important role in a variety of cellular activities, including proliferation, differentiation and apoptosis. Here, we provide a review of the recent work conducted to investigate the function of Ca 2+ signaling in the self-renewal and the neural differentiation of ESCs. Specifically, we describe the role of intracellular Ca 2+ mobilization mediated by RyRs (ryanodine receptors); by cADPR (cyclic adenosine 5'-diphosphate ribose) and CD38 (cluster of differentiation 38/cADPR hydrolase); and by NAADP (nicotinic acid adenine dinucleotide phosphate) and TPC2 (two pore channel 2). We also discuss the Ca 2+ influx mediated by SOCs (store-operated Ca 2+ channels), TRPCs (transient receptor potential cation channels) and LTCC (L-type Ca 2+ channels) in the pluripotent ESCs as well as in neural differentiation of ESCs. Moreover, we describe the integration of Ca 2+ signaling in the other signaling pathways that are known to regulate the fate of ESCs.

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“…When ER [Ca 2+ ] drops, the Ca 2+ -sensing STIM proteins promote Ca 2+ -channel formation (Luik et al, 2008). Blocking this ER-mediated Ca 2+ -entry affects neuronal activity and under conditions of chronic hyperexcitability, STIM proteins are upregulated (Steinbeck et al, 2011). Contributions to electrophysiological excitation-mediated Ca 2+ transients from ER Ca 2+ release have been documented in motoneurons (Scamps et al, 2004, Jahn et al, 2006.…”

Section: Protein Degradation and Endoplasmic Reticulum Stressmentioning

confidence: 99%

Molecular and Electrical Abnormalities in the Mouse Model of Amyotrophic Lateral Sclerosis

Quinlan¹,

Elbasiouny²,

Heckman³

2012

Amyotrophic Lateral Sclerosis

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Store-operated calcium entry modulates neuronal network activity in a model of chronic epilepsy

Cited by 70 publications

References 36 publications

Loss of endoplasmic reticulum Ca2+ homeostasis: contribution to neuronal cell death during cerebral ischemia

Loss of endoplasmic reticulum Ca2+ homeostasis: contribution to neuronal cell death during cerebral ischemia

The role of Ca2+ signaling on the self-renewal and neural differentiation of embryonic stem cells (ESCs)

Molecular and Electrical Abnormalities in the Mouse Model of Amyotrophic Lateral Sclerosis

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