Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/57589
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Type: Journal article
Title: Are the transient receptor potential melastatin (TRPM) channels important in magnesium homeostasis following traumatic brain injury?
Author: Cook, N.
Van Den Heuvel, C.
Vink, R.
Citation: Magnesium Research, 2009; 22(4):225-234
Publisher: John Libbey & Co Ltd
Issue Date: 2009
ISSN: 0953-1424
1952-4021
Statement of
Responsibility: 
Naomi L. Cook, Corinna Van Den Heuvel, Robert Vink
Abstract: Traumatic brain injury (TBI) confers a major burden to Western society and effective treatments are urgently required to improve the long-term deficits that inflict TBI survivors. Depletion of intracellular Mg ²⁺ is a well-known phenomenon occurring after TBI and is associated with poor neurological outcome. However, despite success in pre-clinical experimental studies, therapies utilizing Mg ²⁺ have not always proven to be clinically effective. Recent evidence implicates members of the transient receptor potential melastatin (TRPM) channel family in processes leading to neuronal cell death following ischemic injury, however, the exact mechanism by which this occurs is not completely understood. Specifically, TRPM7 and TRPM6 are two channels that have been identified as potentially playing a role in regulating Mg ²⁺ homeostasis, although whether this role in magnesium regulation and neuronal injury is significant is controversial. The purpose of this review is to explore the relationship between TRPM family members and Mg ²⁺ homeostasis, including their potential involvement in secondary injury processes leading to cell death following TBI.
Keywords: neurotrauma
ischemia
magnesium transporters
free magnesium
calcium
DOI: 10.1684/mrh.2009.0189
Grant ID: NHMRC
Published version: http://dx.doi.org/10.1684/mrh.2009.0189
Appears in Collections:Aurora harvest 5
Pathology publications

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