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Microcalcification after excitotoxicity is enhanced in transgenic mice expressing parvalbumin in all neurones, may commence in neuronal mitochondria and undergoes structural modifications over time

Maetzler, W. and Stünitz, H. and Bendfeldt, K. and Vollenweider, F. and Schwaller, B. and Nitsch, C.. (2009) Microcalcification after excitotoxicity is enhanced in transgenic mice expressing parvalbumin in all neurones, may commence in neuronal mitochondria and undergoes structural modifications over time. Neuropathology and applied neurobiology : journal of the British Neuropathological Society, Vol. 35. pp. 165-177.

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Official URL: http://edoc.unibas.ch/dok/A6005653

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Abstract

AIMS: Parenchymal microcalcification in the brain coincides with neurodegenerative diseases, but is also frequently found in neurologically normal individuals. The origin and role of this process are still under debate. Parvalbumin (PV) is a protein acting as a Ca(2+) buffer and Ca(2+) shuttle towards intracellular Ca(2+) sinks, like mitochondria and the endoplasmic reticulum. Constitutively, it is present in a subset of inhibitory neurones. In transgenic mice expressing pan-neuronal PV, the mitochondrial volume is reduced. We tested whether elevated levels of intraneuronal [Ca(2+)] and reduced mitochondrial volume in the neurone interfere with the generation of parenchymal microcalcification. METHODS: The striatum of wild type and transgenic mice was injected with the glutamate receptor agonist ibotenic acid (IBO), which is known to induce not only excitotoxic neurodegeneration, but also parenchymal calcification. Sections were studied by light and electron microscopy at various time points after IBO application. RESULTS: Morphometric analysis 2, 4 and 20 weeks after IBO application revealed microcalcification in transgenic and wild type mice; the calcification process, however, was enhanced and accelerated in the transgenic animals. Ultrastructural analyses suggest neuronal mitochondria as the nucleators of the deposits which consist of hydroxyapatite. The time-dependent changes in size and surface structure of the deposits indicate the presence of biological mechanisms in the brain promoting regression of bioapatites. CONCLUSIONS: The overload of intraneuronal [Ca(2+)] in combination with impaired mitochondrial function activates neuronal microcalcification. It is hypothesized that this process is an alternative/adaptive mechanism of the neurone to reduce further brain damage.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Division of Anatomy > Cell Adhesion (Spindler)
UniBasel Contributors:Nitsch, Cordula
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Publisher:Blackwell
ISSN:0305-1846
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:24 May 2013 09:22
Deposited On:24 May 2013 09:04

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