VMAT2 and dopamine neuron loss in a primate model of Parkinson’s disease
Article first published online: 6 NOV 2007
© 2007 The Authors
Journal of Neurochemistry
Volume 105, Issue 1, pages 78–90, April 2008
How to Cite
Chen, M.-K., Kuwabara, H., Zhou, Y., Adams, R. J., Brašić, J. R., McGlothan, J. L., Verina, T., Burton, N. C., Alexander, M., Kumar, A., Wong, D. F. and Guilarte, T. R. (2008), VMAT2 and dopamine neuron loss in a primate model of Parkinson’s disease. Journal of Neurochemistry, 105: 78–90. doi: 10.1111/j.1471-4159.2007.05108.x
- Issue published online: 6 NOV 2007
- Article first published online: 6 NOV 2007
- Received September 7, 2007; revised manuscript received October 9, 2007; accepted October 27, 2007.
Fig. S1 TSPO-PET ([11C]-(R)-PK11195) in the baboon brain before and during MPTP administration. Distribution volume (DV) in various brain regions at the different time points. (Error bar = SEM, n = 5). Within a brain region, group means with different letters are significantly different at p < 0.05. Tp = temporal cortex, Pa = parietal cortex, Oc = occipital cortex, Cx = whole cerebral cortex, Po = pons, Cb = cerebellum, Put = putamen, Cd = caudate, Th = thalamus, Fr = frontal cortex.
Fig. S2 Representative images of α-synuclein immunohistochemistry in the substantia nigra (SN) and ventral tegmental (VTA) area of MPTP-treated animals relative to controls. Panels a and b are images from formic acid-treated sections from the VTA (a) and SN (b). Panels c and d are α-synuclein immunohistochemitry without formic acid treatment. Panel c is from the SN of a MPTP-treated animals and panel d from a control animal. There is clear α-synuclein accumulation in VTA and SN neurons from MPTP-treated animals. Scale bar in panels a and b is 10 μm and 30 μm for panels c and d.
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