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THE AUTISM RISK GENE <EM>CNTN4</EM> REGULATES AMPA RECEPTOR EXPRESSION IN NEURONS
Madeline Eveand 2 co-authors
The University of Queensland
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS07-10AM-213
Presentation
Date TBA
Board: PS07-10AM-213
Event Information
Poster Board
PS07-10AM-213
Poster
View posterAbstract
Autism Spectrum Disorder (ASD) is a heterogeneous neurodevelopmental condition that correlates with impairments of the structure and function of synapses. CNTN4 is an autism risk gene that encodes for the synaptic adhesion molecule Contactin 4 (CNTN4). Previous studies have implicated CNTN4 in the regulation of dendritic spine formation and synaptic transmission. However, the mechanism underlying CNTN4 function in synapses remains poorly understood. In this study, we explored the relationship between CNTN4 and the AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid)-type glutamate receptors, which mediate fast excitatory synaptic transmission and are frequently dysregulated in neurodevelopmental disorders. We found that CNTN4 interacts with the GluA1 and GluA2 subunits of AMPARs in primary hippocampal neurons through its fibronectin type III domain. Knockdown of Cntn4 results in the downregulation of surface and total GluA1/2 expression. Importantly, ASD-associated mutations of CNTN4 also resulted in dysregulated GluA2 levels, with a mutation affecting the FNIII domain exhibiting trafficking and GluA2-binding deficits. These findings highlight a previously unknown role of CNTN4 in regulating AMPA receptor function, offering insights into the mechanisms underlying synaptic dysfunction in ASD.
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