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Cerebral Cortex Advance Access originally published online on February 1, 2006
Cerebral Cortex 2007 17(1):28-36; doi:10.1093/cercor/bhj121
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Manganese-Enhanced MRI Reveals Structural and Functional Changes in the Cortex of Bassoon Mutant Mice

Frank Angenstein1,2, Heiko G. Niessen2, Jürgen Goldschmidt1, Holger Lison1, Wilko D. Altrock3, Eckart D. Gundelfinger3 and Henning Scheich1

1 Special Laboratory for Non-invasive Brain Imaging, Leibniz Institute for Neurobiology, Magdeburg, Germany, 2 Department of Neurology II, Otto von Guericke University, Magdeburg, Germany, 3 Department of Neurochemistry and Molecular Biology, Leibniz Institute for Neurobiology, Magdeburg, Germany

Address correspondence to Dr Frank Angenstein, Special Lab Non-invasive Brain Imaging, Leibniz Institute for Neurobiology, Brenneckestrasse 6, 39118 Magdeburg, Germany. Email: angenstein{at}ifn-magdeburg.de.

Manganese-enhanced magnetic resonance imaging (ME-MRI) was used to analyze the brain architecture in mice lacking the functional presynaptic active zone protein Bassoon. Anatomical characterization revealed a significant increase in the total brain volume in Bassoon mutants as compared with wild-type mice, which is mainly caused by changes in cortex and hippocampus volume. The measured enlargement in cortical volume coincides with an altered Mn2+ distribution within cortical layers as visualized by T1-weighted magnetic resonance imaging. Two days after manganese application, the cortex of Bassoon mutant mice appeared more laminated in ME-MRI, with an enhanced accumulation of manganese in deep, central, and superficial cortical cell layers. Whereas morphologically the cortical lamination is not affected by the absence of a functional Bassoon, an altered basal activation pattern was found in the cortex of the mutant mice both by metabolic labeling with [14C]-2-deoxyglucose and histochemical detection of the potassium analogue thallium uptake. Consequently, the results indicate that the absence of the functional presynaptic protein Bassoon causes disturbance in the formation of normal basal cortical activation patterns and thereby in the functional cortical architecture. Furthermore, this study shows that ME-MRI can become a valuable tool for a structural characterization of genetically modified mice.

Key Words: 2-deoxyglucose • hippocampus • thallium autometallography • volumetry


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F. Angenstein, L. Hilfert, W. Zuschratter, W. D. Altrock, H. G. Niessen, and E. D. Gundelfinger
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