RESEARCH ARTICLE


Long-Term Monitoring of Post-Stroke Plasticity After Transient Cerebral Ischemia in Mice Using In Vivo and Ex Vivo Diffusion Tensor MRI



C Granziera*, 1, 2, H D’Arceuil*, #, 1, L Zai3, P.J Magistretti4, A.G Sorensen1, A.J de Crespigny1
1 Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA
2 Department of Neurology, CHUV, Lausanne, Switzerland
3 Laboratories for Neuroscience Research in Neurosurgery, Children’s Hospital, Harvard Medical School, Charlestown, MA, USA
4 Brain Mind Institute, Ecole Polytechnique Federale de Lausanne (EPFL) and Centre de Neurosciences Psychiatriques, Departement de Psychiatrie, CHUV, Lausanne, Switzerland


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2007 Bentham Science Publishers Ltd

* Address correspondence to this author at the Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA; E-mail: helen@nmr.mgh.harvard.edu# Both authors contributed equally to this mauscript.


Abstract

We used a murine model of transient focal cerebral ischemia to study: 1) in vivo DTI long-term temporal evolution of the apparent diffusion coefficient (ADC) and diffusion fractional anisotropy (FA) at days 4, 10, 15 and 21 after stroke 2) ex vivo distribution of a plasticity-related protein (GAP-43) and its relationship with the ex vivo DTI characteristics of the striato-thalamic pathway (21 days).

All animals recovered motor function. In vivo ADC within the infarct was significantly increased after stroke. In the stroke group, GAP-43 expression and FA values were significantly higher in the ipsilateral (IL) striatum and contralateral (CL) hippocampus compared to the shams. DTI tractography showed fiber trajectories connecting the CL striatum to the stroke region, where increased GAP43 and FA were observed and fiber tracts from the CL striatum terminating in the IL hippocampus.

Our data demonstrate that DTI changes parallel histological remodeling and recovery of function.