Relationship between microglial activation and dopaminergic neuronal loss in the substantia nigra: a time course study in a 6-hydroxydopamine model of Parkinson’s disease
Article first published online: 22 JUN 2009
© 2009 The Authors. Journal Compilation © 2009 International Society for Neurochemistry
Journal of Neurochemistry
Volume 110, Issue 3, pages 966–975, August 2009
How to Cite
Marinova-Mutafchieva, L., Sadeghian, M., Broom, L., Davis, J. B., Medhurst, A. D. and Dexter, D. T. (2009), Relationship between microglial activation and dopaminergic neuronal loss in the substantia nigra: a time course study in a 6-hydroxydopamine model of Parkinson’s disease. Journal of Neurochemistry, 110: 966–975. doi: 10.1111/j.1471-4159.2009.06189.x
- Issue published online: 13 JUL 2009
- Article first published online: 22 JUN 2009
- Received May 12, 2009 accepted May 18, 2009.
Figure S1. Injection of 6-OHDA into the mfb resulted in nigrostriatal DA degeneration and expression of OX6+ve cells. 20 μm coronal sections taken at day 9 after 6-OHDA lesion induction were immunostained for TH or OX6 [recognises major histocompatibility complex (MHC) class II antigens]. Panel (a) (left) shows selective loss of TH immunoreactivity ipsilateral to the side of 6-OHDA injection. Neurons in the lateral portion (arrows) and ventral tier (arrowheads) of SNc were most vulnerable. Inserted box illustrates typical cytoplasmic staining in DA neurons (400×). Panel (b) (right) shows specific accumulation of OX6+ve cells at the site of neurodegeneration. Inserted box illustrates typical ramified morphology OX6+ve cells (400×).
Figure S2. Time-dependent unilateral depletion of striatal dopamine content following 6-OHDA lesion induction. Male Sprague–Dawley rats were injected with 12 μg 6-OHDA into the mfb (day 0) and killed at the indicated time points. Striata were removed and processed for HPLC-ECD to measure the striatal dopamine content. Results are expressed as mean (ng/mg) ±SEM. Dopamine deletion manifests from day 9 after 6-OHDA lesion induction and progresses to day 15 after lesioning. **p < 0.01, ***p < 0.001 compared to the non-lesioned side. n = 6 animals/per time point.
Table S1. Confidence intervals for the time dependent changes in the number of OX-42+ve, OX-6+ve and CD68+ve cells in the 6-OHDA lesioned and unlesioned side of the brain.
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