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Acute astrocyte activation in brain detected by MRI: New insights into T1 hypointensity

Lookup NU author(s): Professor Andrew BlamireORCiD

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Abstract

Increases in the T1 of brain tissue, which give rise to dark or hypointense areas on T1-weighted images using magnetic resonance imaging (MRI), are common to a number of neuropathologies including multiple sclerosis (MS) and ischaemia. However, the biologic significance of T 1 increases remains unclear. Using a multiparametric MRI approach and well-defined experimental models, we have experimentally induced increases in tissue T1 to determine the underlying cellular basis of such changes. We have shown that a rapid acute increase in T1 relaxation in the brain occurs in experimental models of both low-flow ischaemia induced by intrastriatal injection of endothelin-1 (ET-1), and excitotoxicity induced by intrastriatal injection of N-methyl-D-aspartate (NMDA). However, there appears to be no consistent correlation between increases in T1 relaxation and changes in other MRI parameters (apparent diffusion coefficient, T 2 relaxation, or magnetisation transfer ratio of tissue water). Immunohistochemically, one common morphologic feature shared by the ET-1 and NMDA models is acute astrocyte activation, which was detectable within 2 h of intracerebral ET-1 injection. Pretreatment with an inhibitor of astrocyte activation, arundic acid, significantly reduced the spatial extent of the T 1 signal change induced by intrastriatal ET-1 injection. These findings suggest that an increase in T1 relaxation may identify the acute development of reactive astrocytes within a central nervous system lesion. Early changes in T1 may, therefore, provide insight into acute and reversible injury processes in neurologic patients, such as those observed before contrast enhancement in MS. © 2008 ISCBFM All rights reserved.

Publication metadata

Author(s): Sibson NR, Lowe JP, Blamire AM, Martin MJ, Obrenovitch TP, Anthony DC

Publication type: Article

Publication status: Published

Journal: Journal of Cerebral Blood Flow and Metabolism

Year: 2008

Volume: 28

Issue: 3

Pages: 621-632

ISSN (print): 0271-678X

ISSN (electronic): 1559-7016

Publisher: Nature Publishing Group

URL: http://dx.doi.org/10.1038/sj.jcbfm.9600549

DOI: 10.1038/sj.jcbfm.9600549

PubMed id: 17851455

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