English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Significance Tuberous Sclerosis Complex (TSC) is a hereditary disease that presents with early brain malformations, childhood epilepsy, and TSC-associated neuropsychiatric disorders (TANDs). Cortical malformations arise in utero and have been linked to childhood epilepsy before. Externally developing zebrafish seem convenient to study elementary neurodevelopment; however, without the in-depth functional analysis, the Tsc2-deficient zebrafish cannot be used for studies of TANDs. Here, we found that Tsc2-deficient zebrafish recapitulated symptoms seen in TSC patients on anatomical and behavioral levels, including aberrant brain morphology, thinning of brain connections, epileptogenesis, and increased anxiety-like behavior, which was rescued by reducing TrkB signaling, revealing a potential drug target. Moreover, we show that commissural thinning cause aberrant regulation of anxiety, providing a link between brain anatomy and emotion.

TrkB hyperactivity contributes to brain dysconnectivity, epileptogenesis, and anxiety in zebrafish model of Tuberous Sclerosis Complex