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Differences in the neurochemical characteristics of the cortex and striatum of mice with cerebral malaria

Published online by Cambridge University Press:  13 December 2004

C. J. CLARK
Affiliation:
Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK
R. S. PHILLIPS
Affiliation:
Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK
R. B. McMILLAN
Affiliation:
Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK
I. O. MONTGOMERY
Affiliation:
Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK
T. W. STONE
Affiliation:
Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK

Abstract

Fatal murine cerebral malaria is an encephalitis and not simply a local manifestation in the brain of a systemic process. Histopathologically, murine cerebral malaria has been characterized by monocyte adherence to the endothelium of the microvasculature, activation of microglial cells, swelling of endothelial cell nuclei, microvasculature damage, and breakdown of the blood-brain barrier with cerebral oedema. Brain parenchymal cells have been proposed to be actively involved in the pathogenesis of murine cerebral malaria. We, therefore, compared the neurochemical characteristics of Plasmodium berghei ANKA-infected mice with controls to determine whether cerebral malarial infection significantly impairs specific neuronal populations. Between 6 and 7 days after infection, we found a significant loss of neurones containing substance P, with preservation of cells containing somatostatin, neuropeptide Y and calbindin in the striatum of infected mice compared with controls. In the cortex of infected mice, we found a significant reduction in the number of cells containing substance P, somatostatin and neuropeptide Y. The number of calbindin-containing neurones was unchanged. This study found significant changes in the neurochemical characteristics of the cortex and striatum of mice infected with P. berghei ANKA, which may contribute to their cerebral symptoms.

Type
Research Article
Copyright
© 2004 Cambridge University Press

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