Abstract
Calcium is the premier messenger molecule mediating adaptive changes in neuroarchitecture in response to signals such as neurotransmitters and neurotrophic factors. Calcium is also involved in long-term adaptive processes, such as memory. Such adaptive changes within an optimal range of intracellular Ca2+ (Ca2+ i) play major roles during development and adult plasticity of the nervous system (1,2). However, when Ca2+ i rises too high and/or for too long a time-period, maladaptive degradation of cellular components can occur. The source of the messenger calcium is either the pool of extracellular Ca2+ ions or calcium sequestered within intracellular pools, such as the endoplasmic reticulum (ER) and mitochondria, or so-called calciosomes (the site for calcium-triggered calcium release) (3). In the former instance calcium homeostasis in the CNS is maintained by Ca2+ entry into neural cells by voltage-sensitive or ligand-gated calcium channels and Ca2+ release from the ER or calciosomes in case of the latter.
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Ye, C., Vassilev, P.M., Chattopadhyay, N. (2003). Expression and Functions of Calcium-Sensing Receptor in the Central Nervous System. In: Chattopadhyay, N., Brown, E.M. (eds) Calcium-Sensing Receptor. Endocrine updates, vol 19. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-9256-7_10
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DOI: https://doi.org/10.1007/978-1-4419-9256-7_10
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