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57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

German Society for Neuropathology and Neuroanatomy

12. - 15.09.2012, Erlangen

57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

Characterisation of glial reactions in the 6-OHDA model of Parkinson’s disease: a time course study

Meeting Abstract

  • presenting/speaker Johannes Schlachetzki - University Hospital Erlangen, Molecular Neurology, Erlangen, Germany
  • Franz Marxreiter - University Hospital Erlangen, Molecular Neurology, Erlangen, Germany
  • Beate Winner - FAU Erlangen-Nuremberg, IZKF Junior Research Group III, Nikoluas-Fiebiger Zentrum, Erlangen, Germany
  • Jürgen Winkler - University Hospital Erlangen, Molecular Neurology, Erlangen, Germany

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. 57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN). Erlangen, 12.-15.09.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. Doc12dgnnPP2.7

DOI: 10.3205/12dgnn043, URN: urn:nbn:de:0183-12dgnn0436

Published: September 11, 2012

© 2012 Schlachetzki et al.
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Outline

Text

Parkinson's disease (PD) is characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) leading to dopaminergic deafferentation in the projection region, the striatum. Glial cells play a crucial role in mediating inflammatory and oxidative processes in PD and may modify the progression of PD. Much is already known about the implication of microglia, the main phagocytic innate immune cells of the brain, in PD pathogenesis. However, the role of astrocytes and oligodendrocytes is far less understood in PD. To this aim, we focused on the glial response in an acute rat model of PD, the 6-hydroxydopamine (6-OHDA) lesion model. To analyze the temporal and spatial pattern of the inflammatory and glial response, unilateral single injection of 6-OHDA into the medial forebrain bundle of 12-week old Wistar rats was performed and analyzed one, two, or six weeks post-lesioning. Striatal deafferentation was already observed one week post-lesioning and progressed until 6 weeks after lesioning. To characterize the microglial response, sections were stained using Iba-1 expression. During the period of 6 weeks, we observed a progressive increase of bilateral Iba-1 positive cells in the striatum. Microglial phenotype changed from a "resting", surveying character to an activated, phag ocytic state in 6-OHDA lesioned animals. A moderate but not significant increase in the number of GFAP-positive astrocytes was observed in the striatum of lesioned rats at all time points. In contrast, no changes in GST-pi positive oligodendrocytes regarding morphology and number were observed at neither of the time points analyzed. Our data suggest that microglia represent the main glial population for developing disease-modifying therapeutic approaches in PD.