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| Content Provider | PubMed Central |
|---|---|
| Author | Kawamoto, Elisa Mitiko Vivar, Carmen Simonetta, Camandola |
| Copyright Year | 2012 |
| Abstract | Calcium (Ca2+) plays fundamental and diversified roles in neuronal plasticity. As second messenger of many signaling pathways, Ca2+ as been shown to regulate neuronal gene expression, energy production, membrane excitability, synaptogenesis, synaptic transmission, and other processes underlying learning and memory and cell survival. The flexibility of Ca2+ signaling is achieved by modifying cytosolic Ca2+ concentrations via regulated opening of plasma membrane and subcellular Ca2+ sensitive channels. The spatiotemporal patterns of intracellular Ca2+ signals, and the ultimate cellular biological outcome, are also dependent upon termination mechanism, such as Ca2+ buffering, extracellular extrusion, and intra-organelle sequestration. Because of the central role played by Ca2+ in neuronal physiology, it is not surprising that even modest impairments of Ca2+ homeostasis result in profound functional alterations. Despite their heterogeneous etiology neurodegenerative disorders, as well as the healthy aging process, are all characterized by disruption of Ca2+ homeostasis and signaling. In this review we provide an overview of the main types of neuronal Ca2+ channels and their role in neuronal plasticity. We will also discuss the participation of Ca2+ signaling in neuronal aging and degeneration. |
| Related Links | http://dx.doi.org/10.3389/fphar.2012.00061 |
| Starting Page | 61 |
| File Format | |
| ISSN | 16639812 |
| e-ISSN | 16639812 |
| Journal | Frontiers in Pharmacology |
| Volume Number | 3 |
| Language | English |
| Publisher | Frontiers Research Foundation |
| Publisher Date | 2012-01-01 |
| Access Restriction | Open |
| Rights Holder | Frontiers Research Foundation |
| Subject Keyword | Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology Pharmacology (medical) |
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