Decreased expression of GLT-1 in the R6/2 model of Huntington's disease does not worsen disease progression
Version of Record online: 16 APR 2013
© 2013 Federation of European Neuroscience Societies and John Wiley & Sons Ltd
European Journal of Neuroscience
Volume 38, Issue 3, pages 2477–2490, August 2013
How to Cite
Petr, G. T., Schultheis, L. A., Hussey, K. C., Sun, Y., Dubinsky, J. M., Aoki, C. and Rosenberg, P. A. (2013), Decreased expression of GLT-1 in the R6/2 model of Huntington's disease does not worsen disease progression. European Journal of Neuroscience, 38: 2477–2490. doi: 10.1111/ejn.12202
- Issue online: 4 AUG 2013
- Version of Record online: 16 APR 2013
- Manuscript Accepted: 26 FEB 2013
- Manuscript Revised: 17 FEB 2013
- Manuscript Received: 17 DEC 2012
- National Institutes of Health Grants
- Hereditary Disease Foundation Postdoctoral Fellowship. Grant Numbers: NS066019, HD18655
Fig. S1. Synaptosomes isolated from the forebrain of wild-type animals are functionally active. A – The association of [3H]-glutamate over time with isolated synaptosomes in the presence of sodium (closed squares) or choline (open triangles). B – The association of [3H]-glutamate with isolated synaptosomes in the presence (open triangles) and absence (closed squares) of 300 μm TBOA. C – Glutamate uptake over time in the absence (closed squares) and presence (open triangles) of 250 μg/ml of saponin. D – Histograms showing the average glutamate uptake into synaptosomes over 30 secs at 0 ºC, 22 ºC and 37ºC. ±SEM; n = 3.
Fig. S2. Saturation analysis of glutamate uptake into the synaptosomal preparations. A – Nonlinear regression analysis demonstrating the association of [3H]-glutamate with synaptosomes isolated from wild-type forebrain in the presence of increasing concentrations of glutamate (closed squares). ±SEM; n = 3 B – Double-reciprocal Lineweaver-Burk plot linearizing rate of glutamate uptake with increasing concentration of glutamate.
Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.