Detailed Information on Publication Record
2021
Changes of blood-cerebrospinal fluid barrier after peripheral nerve injury
LAKATOSOVÁ, Klaudia, Peter SOLÁR, Marek JOUKAL and Václav BRÁZDABasic information
Original name
Changes of blood-cerebrospinal fluid barrier after peripheral nerve injury
Name (in English)
Changes of blood-cerebrospinal fluid barrier after peripheral nerve injury
Authors
Edition
The 13th Conference of the Czech Neuroscience Society, 2021
Other information
Type of outcome
Prezentace na konferencích
Confidentiality degree
není předmětem státního či obchodního tajemství
Změněno: 5/1/2024 10:02, Mgr. Klaudia Hašanová
Abstract
In English
Peripheral nerve injury can induce inflammatory reactions not only in the corresponding dorsal root ganglions (DRGs) but also in remote structures of the central nervous system (CNS). One possible explanation is that products of Wallerian degeneration from distal part of the damaged nerve might migrate and spread the neuroinflammatory reactions into CNS through the blood-cerebrospinal fluid (BCSF) barrier localized in the choroid plexus of the brain ventricles. Changes of the barrier permeability might be caused by alternation of tight junctions (TJs) of epithelial cells in CP leading to disruption of the BCSF barrier. To test the tightness of the BCSF barrier following nerve injury, we intravenously injected the FluoroEmerald (FE) with subsequent analyzes in the cerebrospinal fluid (CSF). In-vivo experiments were performed on 66 Wistar male rats. Animals were divided in 3 groups – rats with sterile chronic constriction injury (sCCI) (n=31), sham-operated rats (n=28) and naive group (n=7). The sCCI and sham-operated were left to survive for 3, 7, 14 and 21 days. After time of survival, we injected the FE and its blood circulation was 30 minutes and 5 hours in each group. The sample of CSF (50ml) without blood contamination and blood from heart were taken and frozen in liquid nitrogen. FE concentration in the CSF and blood samples were assessed by ELISA reader. Subsequently, the animals were transcardially perfused by Zamboni´s fixative and brains were removed. Immunohistochemical staining of ED1, ED2, OX-42, OX-52 and MHC-II were performed on the cryostat sections through the brain ventricles. The analysis of CSF after sCCI and FE administration showed, that FE penetrated the BCSF barrier. The highest concentration of FE in CSF was in sample from animals 3 and 7 days after nerve injury and after 30 minutes of FE circulation. FE was presented in epiplexal Kolmer cells (KC), but also inside ventricular ependymal cells. FE positive KC were simultaneously positive for ED1, ED2, MHC-II, OX-42 and OX-52. Increased FE concentration in the CSF 3 and 7 days after nerve injury suggest alteration of the BCSF barrier and changes in the permeability of the barrier. It was demonstrated that population of FE+ KC is formed by cells with different immunophenotypes. Therefore, we might consider KC as scavenger cells processing penetration of the harmful substances from blood to CSF.
Links
| MUNI/A/1520/2020, interní kód MU |
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