#Calcium entry in neurons dendrite free#
Under resting conditions neurons actively maintain a steep gradient between low intracellular free Ca 2+ concentration i (0.1–0.5 μM) and high extracellular Ca 2+ levels (∼1 mM). The specificity of various biological outcomes is rendered possible by a complex protein network tightly regulating the amplitude, spatial, and temporal patterns of calcium movements through the neuronal cellular compartments. As ubiquitous second messenger, Ca 2+ has been shown to regulate gene expression ( Berridge, 1998), membrane excitability ( Sudhof, 2004), dendrite development ( Lohmann and Wong, 2005 Redmond and Ghosh, 2005), synaptogenesis ( Michaelsen and Lohmann, 2010), and many other processes contributing to the neuronal primary functions of information processing and memory storage ( Berridge, 1998 Tanaka et al., 2008). For example, by regulating the release of neurotransmitters from the presynaptic terminals it influences both long-term potentiation (LTP Grover and Teyler, 1990 Impey et al., 1996) and long-term depression (LTD Bolshakov and Siegelbaum, 1994 Christie et al., 1996) forms of synaptic plasticity. We will also discuss the participation of Ca 2+ signaling in neuronal aging and degeneration.Ĭalcium (Ca 2+) plays fundamental and diversified roles in neuronal physiology. In this review we provide an overview of the main types of neuronal Ca 2+ channels and their role in neuronal plasticity. Despite their heterogeneous etiology neurodegenerative disorders, as well as the healthy aging process, are all characterized by disruption of Ca 2+ homeostasis and signaling. Because of the central role played by Ca 2+ in neuronal physiology, it is not surprising that even modest impairments of Ca 2+ homeostasis result in profound functional alterations. The spatiotemporal patterns of intracellular Ca 2+ signals, and the ultimate cellular biological outcome, are also dependent upon termination mechanism, such as Ca 2+ buffering, extracellular extrusion, and intra-organelle sequestration. The flexibility of Ca 2+ signaling is achieved by modifying cytosolic Ca 2+ concentrations via regulated opening of plasma membrane and subcellular Ca 2+ sensitive channels.
As second messenger of many signaling pathways, Ca 2+ 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. Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, Baltimore, MD, USAĬalcium (Ca 2+) plays fundamental and diversified roles in neuronal plasticity.
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