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Dissertation zugänglich unter
URN: urn:nbn:de:gbv:18-31028
URL: http://ediss.sub.uni-hamburg.de/volltexte/2006/3102/


Quantitative Morphological Analyses of the Striatum and Cerebellum of Tenascin-R deficient mice

Steen, Ann-Britt

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Basisklassifikation: 44.90 , 44.34 , 44.30
Institut: Medizin
DDC-Sachgruppe: Medizin, Gesundheit
Dokumentart: Dissertation
Hauptberichter: Schachner, Melitta (Prof. Dr.)
Sprache: Englisch
Tag der mündlichen Prüfung: 27.10.2006
Erstellungsjahr: 2006
Publikationsdatum: 13.11.2006
Kurzfassung auf Englisch: Tenascin-R is a glycoprotein of the extracellular matrix of the centralnervous system. It is expressed by oligodendrocytes, horizontal cells of the retina and some other neuronal cell populations. It is an essential component for the perineuronal nets around motoneurons and interneurons for example.
The Tenascin-R deficient mouse have a range of behavioural and physiological abnormalities and impaired motor coordination.
This study was designed to further characterize the Tenascin-R deficient mouse with respect to morphological abnormalities in the brain structure known to be involved in motor coordination. Performed were morphological analyses and stereological estimations of immunohistochemical identified major cell types.
The Tenascin-R deficient mouse show normal numbers of different cell types with some exeptions: in the striatum was found a slight increase of microglia in adult Tenascin-R deficient mice and also an increase of parvalbumin positive interneurons in old Tenascin-R deficient mice. In the cerebellum was found an increase of parvalbumin positive interneurons (stellate, basket and Golgi-cells) in adult and old Tenascin-R deficient mice. There is also a genotype-unrelated increase of astrocytes in the striatum and cerebellum and a loss of neurons in the striatum with age.
The results of this study show that deficient expression of Tenascin-R leads to the formation of abnormally large populations of interneurons in the cerebellum. These findings suggest a novel role of Tenascin-R in regulating size of cell populations that normally expressed it during their formation. The motor deficits previously observed in Tenascin-R deficient mice may be related to abnormal interneuron populations in the cerebellum.

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