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Changes in Magnetization Transfer MRI Correlate with Spreading Depression–Induced Astroglial Reactivity and Increased Protein Expression in Mice

Christopher D. Lascola1,2, Allen W. Song1,2, Timothy A. Haystead3,4, David S. Warner5, Katleen Verleysen4, Tiffany A. Freed4 and James M. Provenzale1

1 Department of Radiology, Duke University Medical Center, Box 3808, Durham, NC 27710.
2 Brain Imaging and Analysis Center, Duke University Medical Center, Durham, NC 27710.
3 Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710.
4 Serenex, Inc., Durham, NC.
5 Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710.



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  		Fig. 1A. —Drawings show recording of spreading depression in mouse cerebral hemispheres. Electrophysiologic traces show DC extracellular potential recordings from experimental (right) and control (left) cerebral hemispheres. Spreading depression was elicited by focal application of KCl to right occipital cortical surface. Spreading depression was never observed in contralateral control neocortex.

 


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  		Fig. 1B. —Drawings show recording of spreading depression in mouse cerebral hemispheres. Pair of traces represent 30-min interval of recurrent spreading depression, while simultaneously measuring relative blood flow (higher trace) and DC potential deflections (lower trace) using dural surface electrode. Blood flow changes were measured with transcranial laser Doppler probe and DC potentials with silver chloride ball electrode applied directly to brain surface. Mean ± SD of 16 ± 3 spreading depressions were recorded (n = 10) in right cerebral hemisphere over 2-hr period.

 


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  		Fig. 2A. —Magnetization transfer MRI of mouse brain 3 days after spreading depression. Gray-scale magnetization transfer image shows representative coronal 1.5-mm slice, 3.0 mm from site of KCl application. Note slight decrease in signal intensity in right cerebral hemisphere compared with left.

 


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  		Fig. 2B. —Magnetization transfer MRI of mouse brain 3 days after spreading depression. Magnetization transfer image (A) after color lute has been overlaid on gray-scale image shows decrease in signal intensity involving right cerebral hemisphere relative to left.

 


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  		Fig. 2C. —Magnetization transfer MRI of mouse brain 3 days after spreading depression. Magnetization transfer image (based on A and B) shows regions of interest drawn around each cerebral hemisphere for calculation of mean signal intensity values. Regions of interest include cortical gray and white matter of each hemisphere, separated from underlying hippocampus.

 


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  		Fig. 2D. —Magnetization transfer MRI of mouse brain 3 days after spreading depression. Bar graph shows 8% decrease (p < 0.05, n = 4) in magnetization transfer signal intensity compared with control hemisphere 3 days after spreading depression (SD).

 


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  		Fig. 3A. —Glial fibrillary acidic protein immunohistochemistry of mouse brain 3 days after spreading depression. Photomicrograph of histopathologic specimen shows glial fibrillary acidic protein-stained astrocytes in contralateral control cortex.

 


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  		Fig. 3B. —Glial fibrillary acidic protein immunohistochemistry of mouse brain 3 days after spreading depression. Photomicrograph of histopathologic specimen shows reactive glial fibrillary acidic protein-stained astrocytes. Note increase in size of cell bodies and increased number of glial fibrillary acidic protein-stained cellular processes.

 


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  		Fig. 3C. —Glial fibrillary acidic protein immunohistochemistry of mouse brain 3 days after spreading depression. Bar graph shows 37% increase in glial fibrillary acidic protein (GFAP) staining in right hemisphere (Control) as compared with left (spreading depression [SD], n = 4, p < 0.001) 3 days after spreading depression.

 


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  		Fig. 4A. —Proteomic analysis of spreading depression–induced changes in neocortex of mouse 3 days after spreading depression. Polyacrylamide one-dimensional electrophoresis gel of left (control) cerebral tissue homogenate after fractionization 3 days after spreading depression. Individual bands represent proteins from control cortex.

 


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  		Fig. 4B. —Proteomic analysis of spreading depression–induced changes in neocortex of mouse 3 days after spreading depression. Polyacrylamide one-dimensional electrophoresis gel of right (experimental) cortex after fractionization 3 days after spreading depression. At least 56 upregulated or newly expressed protein bands in experimental hemisphere are shown. Mass analysis matrix-assisted laser desorption/ionization time-of-flight mass spectroscopy identified half of upregulated proteins, which include extra- and intracellular structural components, metabolic proteins, kinases, and other miscellaneous gene products: (4) collagen alpha chain precursor, (5) clathrin heavy chain, (12) T complex protein delta, (15) vacuolar adenosine triphosphate synthetase subunit A, (17) syntaxin-binding protein, (21) tubulin, (22) calcium-calmodulin-dependent protein kinase type II, (23) tubulin, (24) phosphoglycerate kinase, (25) actin, (27) fructose bisphosphonate aldolase, (31) glyceraldehyde-3-phosphate dehydrogenase, (32) malate dehydrogenase (syntaxin 1A), (36) vacuolar adenosine triphosphate synthetase subunit E, (40) glutathione S-transferase P1, (41) superoxide dismutase precursor, (44) cofilin, (46) peptidyl-prolyl cis-trans isomerase, (47) heat shock protein 70, (49) phosphatidylinositol transfer protein alpha isoform, (50) F-actin capping protein alpha isoform, and (53) creatine kinase.

 

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