Published October 31, 2019
| Version v1
Dataset
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Impaired dopamine- and adenosine-mediated signaling and plasticity in a novel rodent model for DYT25 dystonia
Creators
- 1. Institute of Medical Genetics and Applied Genomics, and Centre for Rare Diseases (ZSE), University of Tuebingen, Tuebingen, Germany
- 2. Institute of Medical Genetics and Applied Genomics, and Core Facility Transgenic Animals, University Tuebingen, Tuebingen, Germany
- 3. Laboratory of Neurophysiology and Plasticity, IRCCS Fondazione Santa Lucia, Rome, Italy
- 4. Center for the Biology of Disease/ Laboratory of Dystonia Research, Catholic University of Leuven, Leuven, Belgium
- 5. Institute of Medical Genetics and Applied Genomics, University of Tuebingen, Tuebingen, Germany; Department of Human Genetics, Faculty of Medicine, Ruhr University Bochum, Bochum, Germany
Description
Raw data of Figure 5 - (D) Summary plots of Tau values (left) and AMPA/NMDA ratio (right), measured from Gnal+/+ and Gnal+/- EPSCs showing no significant difference between genotypes (Tau: Gnal+/+, 9.47 ± 0.50 ms, n=31; Gnal+/-, 10.05 ± 0.66 ms, n=27; p=0.4832; AMPA/NMDA ratio: Gnal+/+ , 1.27 ± 0.14, n=10; Gnal+/-, 1.24 ± 0.13, n=15; Mann Whitney test p=0.9779). (E) Summary plot of PPR values showing similar facilitation in both genotypes. Each data point represents mean ± SEM (Gnal+/+, n=30, 50 ms: 1.22 ± 0.04; 100 ms: 1.16 ± 0.03; 150 ms: 1.11 ± 0.40; Gnal+/-, n=25, 50 ms: 1.28 ± 0.03; 100 ms: 1.17 ± 0.03; 150 ms: 1.09 ± 0.02; two-way ANOVA and Bonferroni posttest: ISI p<0.0001, genotype p=0.2405).
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Additional details
Related works
- Is supplement to
- Journal article: 10.1016/j.nbd.2019.104634 (DOI)