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Image Search Results
Journal: PLoS genetics
Article Title: FUS transgenic rats develop the phenotypes of amyotrophic lateral sclerosis and frontotemporal lobar degeneration.
doi: 10.1371/journal.pgen.1002011
Figure Lengend Snippet: Figure 4. Neuron loss accompanied by ubiquitin aggregation in aged rats overexpressing the normal human fus gene. (A–C) Double- fluorescence staining for human FUS (A, red) and the neuronal marker NeuN (B, green) in the frontal cortex of normal human FUS transgenic rats (line 20). Most FUS-positive cells expressed NeuN, but some did not (C). (D–I) Immunofluorescence staining revealed ubiquitin aggregation in aged (G–I; 1 year of age), but not young (D–F; 3 months of age), normal FUS transgenic rats. Coronal sections of frontal cortex were immunostained with antibodies to ubiquitin (D, G: green) and human FUS (E, H: red). Scale bars: A–C, 100 mm; D–I, 20 mm. (J, K) Barnes maze analysis revealed spatial learning deficits in normal FUS transgenic rats of line 20 at advanced ages. One year old transgenic rats (TG) and their nontransgenic littermates (NT) were tested in a Barnes maze and time spent to locate the fixed escape hole (latency) and the number of errors made before escaping were recorded. (L, M) Stereological cell counting revealed a loss of neurons in the cortex (J) and dentate gyrus (K) of normal FUS transgenic rats at advanced ages (line 20). Coronal sections of one hemisphere were stained with Cresyl violet and the number of neurons in the frontal cortex and dentate gyrus was estimated by stereological cell counting. Normal FUS transgenic rats and their nontransgenic controls were killed at the age of 1 year. Data are presented as means 6 SD (n = 5). * p,0.05. doi:10.1371/journal.pgen.1002011.g004
Article Snippet: Spatial learning and memory tasks were examined with a
Techniques: Ubiquitin Proteomics, Fluorescence, Staining, Marker, Transgenic Assay, Immunofluorescence, Cell Counting