» Articles » PMID: 28900932

Neurological and Motor Disorders: Neuronal Store-Operated Ca Signaling: An Overview and Its Function

Overview
Date 2017 Sep 14
PMID 28900932
Citations 17
Authors
Affiliations
Soon will be listed here.
Abstract

Calcium (Ca) is a ubiquitous second messenger that performs significant physiological task such as neurosecretion, exocytosis, neuronal growth/differentiation, and the development and/or maintenance of neural circuits. An important regulatory aspect of neuronal Ca homeostasis is store-operated Ca entry (SOCE) which, in recent years, has gained much attention for influencing a variety of nerve cell responses. Essentially, activation of SOCE ensues following the activation of the plasma membrane (PM) store-operated Ca channels (SOCC) triggered by the depletion of endoplasmic reticulum (ER) Ca stores. In addition to the TRPC (transient receptor potential canonical) and the Orai family of ion channels, STIM (stromal interacting molecule) proteins have been baptized as key molecular regulators of SOCE. Functional significance of the TRPC channels in neurons has been elaborately studied; however, information on Orai and STIM components of SOCE, although seems imminent, is currently limited. Importantly, perturbations in SOCE have been implicated in a spectrum of neuropathological conditions. Hence, understanding the precise involvement of SOCC in neurodegeneration would presumably unveil avenues for plausible therapeutic interventions. We thus review the role of SOCE-regulated neuronal Ca signaling in selecting neurodegenerative conditions.

Citing Articles

Combined treatment targeting Ca2+ store mediated Ca2+ release and store-operated calcium entry reduces secondary axonal degeneration and improves functional outcome after SCI.

Jones E, Ames S, Brooks J, Morehouse J, Hill N, Mikoshiba K Exp Neurol. 2025; 386:115178.

PMID: 39909217 PMC: 11875899. DOI: 10.1016/j.expneurol.2025.115178.


Calcium Ions in the Physiology and Pathology of the Central Nervous System.

Pikor D, Hurla M, Slowikowski B, Szymanowicz O, Poszwa J, Banaszek N Int J Mol Sci. 2024; 25(23).

PMID: 39684844 PMC: 11642227. DOI: 10.3390/ijms252313133.


A bright cyan fluorescence calcium indicator for mitochondrial calcium with minimal interference from physiological pH fluctuations.

Gu W, Yang Y, Wang Y, Li J, Li W, Zhang X Biophys Rep. 2024; 10(5):315-327.

PMID: 39539283 PMC: 11554577. DOI: 10.52601/bpr.2024.240001.


Highly efficient Ca chelation activated by visible light.

Egodawaththa N, Rajhel O, Ma J, Guruge C, Pabarue A, Harris E Org Biomol Chem. 2024; 22(35):7194-7202.

PMID: 39161284 PMC: 11717440. DOI: 10.1039/d4ob00951g.


A Review of the Gene Family: Its Role in Neurological Disorders.

Szymanowicz O, Druzdz A, Slowikowski B, Pawlak S, Potocka E, Goutor U Diseases. 2024; 12(5).

PMID: 38785745 PMC: 11119137. DOI: 10.3390/diseases12050090.


References
1.
Dulneva A, Lee S, Oliver P, Di Gleria K, Kessler B, Davies K . The mutant Moonwalker TRPC3 channel links calcium signaling to lipid metabolism in the developing cerebellum. Hum Mol Genet. 2015; 24(14):4114-25. PMC: 4476454. DOI: 10.1093/hmg/ddv150. View

2.
Balzer M, Lintschinger B, Groschner K . Evidence for a role of Trp proteins in the oxidative stress-induced membrane conductances of porcine aortic endothelial cells. Cardiovasc Res. 1999; 42(2):543-9. DOI: 10.1016/s0008-6363(99)00025-5. View

3.
Sattler R, Tymianski M . Molecular mechanisms of calcium-dependent excitotoxicity. J Mol Med (Berl). 2000; 78(1):3-13. DOI: 10.1007/s001090000077. View

4.
Bojarski L, Pomorski P, Szybinska A, Drab M, Skibinska-Kijek A, Gruszczynska-Biegala J . Presenilin-dependent expression of STIM proteins and dysregulation of capacitative Ca2+ entry in familial Alzheimer's disease. Biochim Biophys Acta. 2008; 1793(6):1050-7. DOI: 10.1016/j.bbamcr.2008.11.008. View

5.
Henke N, Albrecht P, Bouchachia I, Ryazantseva M, Knoll K, Lewerenz J . The plasma membrane channel ORAI1 mediates detrimental calcium influx caused by endogenous oxidative stress. Cell Death Dis. 2013; 4:e470. PMC: 3564003. DOI: 10.1038/cddis.2012.216. View