Publikationsdatenbank

The role of adult neurogenesis during epileptogenesis in a viral encephalitis-induced seizure model (2025)

Art

Poster

Autoren

Weiß, Edna (WE 14)

Pauletti, Alberto (WE 14)

Egilmez, Asya (WE 14)

Bröer, Sonja (WE 14)

Kongress

11th Eilat Educational Course : pharmacological treatment of epilepsy

Limassol, Cyprus, 12. – 17.10.2025

Quelle

11th Eilat International Educational Course : Abstracts

— S. 9

Sprache

Englisch

Verweise

URL (Volltext): https://events.eventact.com/comtec/36949/WebSitePage/uploads/all_abstracts_for_website-2.pdf?webid=16969684913

Kontakt

Institut für Pharmakologie und Toxikologie

Koserstr. 20
14195 Berlin
+49 30 838 53221
pharmakologie@vetmed.fu-berlin.de

Abstract / Zusammenfassung

Neurogenesis, the generation of new nerve cells, is disrupted in traditional rodent epilepsy models, and altered cell maturation and migration contribute to hyperexcitability and cognitive impairment. Very little is known about the impact of encephalitis-derived seizures on neural stem cells (NSCs) and their differentiation after infections of the central nervous system (CNS), although CNS infections are one of the major causes of seizures. We are aiming to identify treatment windows for modulating neurogenesis to modify epileptogenesis after CNS infection.
The Theiler’s murine encephalomyelitis virus (TMEV) model is a translational mouse model that simulates infection-triggered acute, and chronic, unprovoked seizures. An intracortical, unilateral injection of the Daniel’s strain of Theilervirus induces seizures in 50-75% C57BL6 mice within the first week, and about 25% of mice develop chronic epilepsy. Mice were sacrificed at 7-, 14-, 28- and 90 days post infection (dpi) to evaluate neurogenesis in the subgranular layer of the hippocampal dentate gyrus.
TMEV infection rapidly depleted subgranular immature neurons (DCX+), with mice experiencing seizures demonstrating a more pronounced reduction in neuronal progenitor cell density. Additionally, seizures induced ectopic migration of surviving neuronal progenitors at 14 dpi. On the contrary, proliferating microglia and astrocytes were significantly increased in TMEV infected animals depending on the timepoint.
Ongoing long-term fate tracking of progenitor cells by BrdU labelling in 28 dpi and 90 dpi animals will reveal the fate and migration patterns of NSCs within the hippocampus over the disease course, and determine their role in seizure development.