Neuronal calcium signaling via store-operated channels in health and disease

• Published in: Cell calcium (Edinburgh) 2018-09, Vol.74, p.102-111
• Main Authors: Wegierski, Tomasz, Kuznicki, Jacek
• Format: Article
• Language: English
• Subjects: Animals; Calcium Signaling - physiology; Capacitative calcium entry (CCE); Hippocampus - metabolism; Hippocampus - pathology; Humans; Neoplasm Proteins - metabolism; Neurodegenerative disease; Neurodegenerative Diseases - metabolism; Neurodegenerative Diseases - pathology; Neuronal Plasticity - physiology; Neuronal store operated calcium entry (nSOCE); Neurons - metabolism; Neurons - pathology; Orai; ORAI1 Protein - metabolism; STIM; Stromal Interaction Molecule 1 - metabolism; Traumatic brain injury
• ISSN: 0143-4160; 1532-1991
• DOI: 10.1016/j.ceca.2018.07.001

[Display omitted] •Neuronal store-operated calcium entry (nSOCE) was detected in multiple brain areas.•nSOCE is required for neuronal physiology.•Dysregulation of nSOCE is observed in pathologies, such as AD, HD, PD, and TBI.•Molecular components of nSOCE are possible targets for therapeutic interventions. Store-operated calcium entry (SOCE) is the flow of calcium ions (Ca2+) into cells in response to the depletion of intracellular Ca2+ stores that reside predominantly in the endoplasmic reticulum (ER). The role of SOCE has been relatively well understood for non-excitable cells. It is mediated mostly by the ER Ca2+ sensor STIM1 and plasma membrane Ca2+ channel Orai1 and serves to sustain Ca2+ signaling and refill ER Ca2+ stores. In contrast, because of the complexity of Ca2+ influx mechanisms that are present in excitable cells, our knowledge about the function of neuronal SOCE (nSOCE) is still nascent. This review summarizes the available data on the molecular components of nSOCE and their relevance to neuronal signaling. We also present evidence of disturbances of nSOCE in neurodegenerative diseases (namely Alzheimer’s disease, Huntington’s disease, and Parkinson’s disease) and traumatic brain injury. The emerging important role of nSOCE in neuronal physiology and pathology makes it a possible clinical target.