Are the transient receptor potential melastatin (TRPM) channels important in magnesium homeostasis following traumatic brain injury?

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.

journal_name

Magnes Res

journal_title

Magnesium research

authors

Cook NL,Van Den Heuvel C,Vink R

doi

10.1684/mrh.2009.0189

subject

Has Abstract

pub_date

2009-12-01 00:00:00

pages

225-34

issue

4

eissn

0953-1424

issn

1952-4021

pii

mrh.2009.0189

journal_volume

22

pub_type

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