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Updated: Aug 23, 2026

Transient Middle Cerebral Artery Occlusion Model of Stroke
Published on: August 11, 2023
In, out, shake it all about: elevation of [Ca2+]i during acute cerebral ischaemia
1Division of Clinical Neurosciences, University of Southampton, Room 6207, Biomedical Sciences Building, Bassett Crescent East, Southampton SO16 7PX, UK. akp1@soton.ac.uk
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.
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