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Stroke Research and Treatment
Volume 2010 (2010), Article ID 316862, 9 pages
Review Article

Modes of Neuronal Calcium Entry and Homeostasis following Cerebral Ischemia

1Centre for Neuromuscular and Neurological Disorders, Australian Neuromuscular Research Institute, University of Western Australia, WA 6009, Australia
2Department of Neurosurgery, Sir Charles Gairdner Hospital, WA 6009, Australia
3School of Biomedical, Biomolecular and Chemical Sciences, University of Western Australia, WA 6009, Australia

Received 7 July 2010; Accepted 29 September 2010

Academic Editor: Byung Woo Yoon

Copyright © 2010 J. L. Cross et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


One of the major instigators leading to neuronal cell death and brain damage following cerebral ischemia is calcium dysregulation. The neuron's inability to maintain calcium homeostasis is believed to be a result of increased calcium influx and impaired calcium extrusion across the plasma membrane. The need to better understand the cellular and biochemical mechanisms of calcium dysregulation contributing to neuronal loss following stroke/cerebral ischemia is essential for the development of new treatments in order to reduce ischemic brain injury. The aim of this paper is to provide a concise overview of the various calcium influx pathways in response to ischemia and how neuronal cells attempts to overcome this calcium overload.