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 Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background Tbr1  encodes a T-box transcription factor and is considered a high confidence autism spectrum disorder (ASD) gene.  Tbr1  is expressed in the postmitotic excitatory neurons of the deep neocortical layers 5 and 6. Postnatally and neonatally,  Tbr1  conditional mutants (CKOs) have immature dendritic spines and reduced synaptic density. However, an understanding of  Tbr1 ’s function in the adult mouse brain remains elusive. Methods We used conditional mutagenesis to interrogate  Tbr1 ’s function in cortical layers 5 and 6 of the adult mouse cortex. Results Adult  Tbr1  CKO mutants have dendritic spine and synaptic deficits as well as reduced frequency of mEPSCs and mIPSCs. LiCl, a WNT signaling agonist, robustly rescues the dendritic spine maturation, synaptic defects, and excitatory and inhibitory synaptic transmission deficits. Conclusions LiCl treatment could be used as a therapeutic approach for some cases of ASD with deficits in synaptic transmission.

LiCl treatment leads to long-term restoration of spine maturation and synaptogenesis in adult Tbr1 mutants