ArticleJournal of neurodevelopmental disorders2022
LiCl treatment leads to long-term restoration of spine maturation and synaptogenesis in adult Tbr1 mutants.
Article in Journal of neurodevelopmental disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Physical and functional convergence of the autism risk genes Scn2a and Ank2 in neocortical pyramidal cell dendrites.Neuron · 2024Article
- Shared and Distinct Functional Effects of Patient-SpecificThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTbr1 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.
methodsWe used conditional mutagenesis to interrogate Tbr1's function in cortical layers 5 and 6 of the adult mouse cortex.
resultsAdult 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.
conclusionsLiCl treatment could be used as a therapeutic approach for some cases of ASD with deficits in synaptic transmission.
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