Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Feb 18;225(2):805–816. doi: 10.1007/s00429-020-02036-3

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 4 — Shown in a is a sagittal section of adult mouse brain depicting examined regions (red circles): cerebral cortex (CX) and cerebellum (CB). Graphs b–d show quantitative RT-PCR of laminin α-1, laminin α-2 and agrin mRNA (copy number/ng of total RNA) from CX and CB, and compare WT with α-Syn−/− genotypes. Analysis of laminin α-1b demonstrates similar levels between CX and CB in WT mice (CX: mean 235.77, SD 92.54 and CB mean 309.96, SD 30.08) which remain unaltered following gene deletion of α-Syn (CX mean 246.53, SD 36.81; CB mean 277.40, SD 9.51). Data for laminin α-2c demonstrate regional differences in WT controls (CX mean 182.22, SD 31.41; CB mean 364.49, SD 29.90) and similar differences are observed in α-Syn−/− mice (CX mean 196.00, SD 28.13 and CB mean 310.80, SD 6.55). Analysis of agrin demonstrates similar regional differences between CX (mean 1861.13; SD 435.95) and CB (mean 964.55; SD 37.76) in α-Syn−/− mice as seen in WT controls (CX: mean 1471.91; SD 236.70 and CB: mean 821.82; SD 67.06). Error bars in b–d represent 95% confidence intervals, calculated by bootstrapping. Figures e–h show quantitative immunogold labelling of agrin and laminin, measured as linear density of gold particles per µm length of the basal lamina. Data are shown as one single column for each basal lamina microdomain or anatomical region. Analysis for both proteins e, f shows no difference between genotypes when examining basal lamina microdomains (endper, end, per). At the regional level, the heterogeneous expression of both laminin and agrin in the basal lamina of the cortical and cerebellar capillary bed thus seems independent of α-Syn. Figures g, h depict quantitative immunogold labelling of capillary basal lamina: Images from sublayers of CB were merged (CB-mol, CB-gran and CB-white). The basal lamina enclosed between pericytes and endothelium (endper) was not included so as to assess influence of astrocytes upon agrin and laminin expression. The remaining basal lamina microdomains were merged as one datapoint per acquired image. Genetic deletion of α-Syn does not impact on the observed regional differences in immunogold labelling (agrin and laminin alike). No difference is found when comparing levels of either protein (agrin or laminin) in WT vs α-Syn−/− genotypes, neither for CX nor for CB. Error bars in e–h represent standard error of the mean (SEM)