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World J Biol Chem. Jul 26, 2010; 1(7): 229-234
Published online Jul 26, 2010. doi: 10.4331/wjbc.v1.i7.229
Plasma membrane Ca2+-ATPases in the nervous system during development and ageing
Ana M Mata, M Rosario Sepulveda
Ana M Mata, M Rosario Sepulveda, Department of Biochemistry and Molecular Biology and Genetics, Faculty of Sciences, University of Extremadura, 06006 Badajoz, Spain
Author contributions: Both authors performed some of the work described in the review and wrote the manuscript.
Supported by Grants No. BFU2008-00182 from MICINN, Fundaci¨®n Marcelino Botín, Spain (to Mata AM); Sepulveda MR received a Postdoctoral Fellowship from Programa de Reincorporaci¨®n de Doctores, Junta de Extremadura, Spain
Correspondence to: Ana M Mata, PhD, Professor, Department of Biochemistry and Molecular Biology and Genetics, Faculty of Sciences, University of Extremadura, 06006 Badajoz, Spain. anam@unex.es
Telephone: +34-924-289418 Fax: +34-924-289419
Received: May 27, 2010
Revised: July 1, 2010
Accepted: July 8, 2010
Published online: July 26, 2010
Abstract

Calcium signaling is used by neurons to control a variety of functions, including cellular differentiation, synaptic maturation, neurotransmitter release, intracellular signaling and cell death. This review focuses on one of the most important Ca2+ regulators in the cell, the plasma membrane Ca2+-ATPase (PMCA), which has a high affinity for Ca2+ and is widely expressed in brain. The ontogeny of PMCA isoforms, linked to specific requirements of Ca2+ during development of different brain areas, is addressed, as well as their function in the adult tissue. This is based on the high diversity of variants in the PMCA family in brain, which show particular kinetic differences possibly related to specific localizations and functions of the cell. Conversely, alterations in the activity of PMCAs could lead to changes in Ca2+ homeostasis and, consequently, to neural dysfunction. The involvement of PMCA isoforms in certain neuropathologies and in brain ageing is also discussed.

Keywords: Calcium; Brain; ATPase; Plasma membrane; Differentiation; Neurodegeneration