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Central Nervous System

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Calcium in Internal Medicine
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Abstract

Calcium ion (Ca2+) is an omnipresent intracellular messenger controlling multiple cell functions such as growth, differentiation, membrane permeability and exocytosis, synaptic activity and gene regulation. In neuronal cells, resting levels of intracellular calcium ([Ca2+]i) are around 50-200 nM, 104 times lower than extracellular Ca2+, which allows them to achieve a high ratio of signal to resting/background [Ca2+] i when [Ca2+] i is suddenly increased. Thus, relatively small, transient and localised increases in [Ca2+]i can induce a physiological response by activation of enzymes, change in membrane channels activity, neurotransmitter release modulation of synaptic transmission, programmed cell death through apoptosis and alteration of gene expression. Under normal conditions, the delicate balance between Ca2+ influx, Ca2+ buffering, intracellular Ca2+ storage and Ca2+ efflux is maintained, preserving wide options for Ca2+ signalling. However, it is currently established that excessive Ca2+ entry or inadequate buffering mechanisms can lead to acute overactivation of neurons or chronic neurotoxicity. The precise mechanisms by which neurotoxicity occurs are still not completely understood, despite the research efforts of the past 30 years.

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Smogorzewski, M. (2002). Central Nervous System. In: Morii, H., Nishizawa, Y., Massry, S.G. (eds) Calcium in Internal Medicine. Springer, London. https://doi.org/10.1007/978-1-4471-0667-8_25

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