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In, out, shake it all about: elevation of [Ca2+]i during acute cerebral ischaemia

In, out, shake it all about: elevation of [Ca2+]i during acute cerebral ischaemia
In, out, shake it all about: elevation of [Ca2+]i during acute cerebral ischaemia
Because of the extensive second messenger role played by calcium, free intracellular calcium levels are strictly regulated. Under normal physiological conditions, this is achieved through a combination of restricted calcium entry, efficient efflux and restricted intracellular mobility. Overall, the process of regulating free calcium is dependent on ATP derived from oxidative metabolism. Under conditions of cerebral ischaemia, ATP levels fall rapidly and calcium homeostasis becomes significantly disturbed resulting in the initiation of calcium-dependent neurodegenerative processes. In this review, the mechanisms underlying physiological calcium homeostasis and the links between calcium disregulation and neurodegeneration will be discussed.
AMPA, ?-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; CBP, calcium-binding protein; ER, endoplasmic reticulum; IP3, inositol-1,4,5-triphosphate; NMDA, N-methyl--aspartate; OGD, oxygen/glucose deprivation; VDCC, voltage-dependent calcium channel
free intracellular calcium, cerebral ischaemia, calcium homeostasis, excitotoxicity, glutamate, voltage-dependent calcium channels
0143-4160
235-245
Pringle, A.K.
6339ed95-c491-43a8-b2fb-2384466dc80d
Pringle, A.K.
6339ed95-c491-43a8-b2fb-2384466dc80d

Pringle, A.K. (2004) In, out, shake it all about: elevation of [Ca2+]i during acute cerebral ischaemia. Cell Calcium, 36 (3-4), 235-245. (doi:10.1016/j.ceca.2004.02.014).

Record type: Article

Abstract

Because of the extensive second messenger role played by calcium, free intracellular calcium levels are strictly regulated. Under normal physiological conditions, this is achieved through a combination of restricted calcium entry, efficient efflux and restricted intracellular mobility. Overall, the process of regulating free calcium is dependent on ATP derived from oxidative metabolism. Under conditions of cerebral ischaemia, ATP levels fall rapidly and calcium homeostasis becomes significantly disturbed resulting in the initiation of calcium-dependent neurodegenerative processes. In this review, the mechanisms underlying physiological calcium homeostasis and the links between calcium disregulation and neurodegeneration will be discussed.
AMPA, ?-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; CBP, calcium-binding protein; ER, endoplasmic reticulum; IP3, inositol-1,4,5-triphosphate; NMDA, N-methyl--aspartate; OGD, oxygen/glucose deprivation; VDCC, voltage-dependent calcium channel

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More information

Published date: 2004
Keywords: free intracellular calcium, cerebral ischaemia, calcium homeostasis, excitotoxicity, glutamate, voltage-dependent calcium channels

Identifiers

Local EPrints ID: 27692
URI: http://eprints.soton.ac.uk/id/eprint/27692
ISSN: 0143-4160
PURE UUID: 56eb7fc9-ab1a-4cfc-9d6d-a8cdfc210225
ORCID for A.K. Pringle: ORCID iD orcid.org/0000-0003-2421-4380

Catalogue record

Date deposited: 27 Apr 2006
Last modified: 16 Mar 2024 02:48

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