ArticleThe Journal of experimental medicine2018
Autism-associated neuroligin-4 mutation selectively impairs glycinergic synaptic transmission in mouse brainstem synapses.
Article in The Journal of experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 45 citations in OpenAlex.
- Article
- Insertion of rare autism variants in synaptic genes induce novel behavioral phenotypes inbioRxiv : the preprint server for biology · 2025Article
- Autism Spectrum Disorder: The Cerebellum, Genes, and Pathways.Neurology international · 2025Review
- Atypical Cadherin FAT2 Is Required for Synaptic Integrity and Motor Behaviors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- The association between NLGN4 gene variants and the incidence of autism spectrum disorders in Guilan, Iran.IBRO neuroscience reports · 2025Article
- Article
- Astrocytic Neuroligin-3 influences gene expression and social behavior, but is dispensable for synapse number.Molecular psychiatry · 2025Article
- Region-Specific Phosphorylation Determines Neuroligin-3 Localization to Excitatory Versus Inhibitory Synapses.Biological psychiatry · 2024Article
- Sex-specific microglia state in the Neuroligin-4 knock-out mouse model of autism spectrum disorder.Brain, behavior, and immunity · 2023Article
- Increased Network Inhibition in the Dentate Gyrus of Adult Neuroligin-4 Knock-Out Mice.eNeuro · 2023Article
- Engineered adhesion molecules drive synapse organization.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Signalling pathways in autism spectrum disorder: mechanisms and therapeutic implications.Signal transduction and targeted therapy · 2022Review
- Molecular self-avoidance in synaptic neurexin complexes.Science advances · 2021Article
- An optogenetic method for investigating presynaptic molecular regulation.Scientific reports · 2021Article
- A paradigmatic autistic phenotype associated with loss of PCDH11Y and NLGN4Y genes.BMC medical genomics · 2021Article
- GABAergic System Dysfunction in Autism Spectrum Disorders.Frontiers in cell and developmental biology · 2021Review
- Functional mosaic organization of neuroligins in neuronal circuits.Cellular and molecular life sciences : CMLS · 2020Review
- A Cluster of Autism-Associated Variants on X-Linked NLGN4X Functionally Resemble NLGN4Y.Neuron · 2020Article
- Neuroligins and Neurodevelopmental Disorders: X-Linked Genetics.Frontiers in synaptic neuroscience · 2020Review
- Elevated Plasma X-Linked Neuroligin 4 Expression Is Associated with Autism Spectrum Disorder.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
In human patients, loss-of-function mutations of the postsynaptic cell-adhesion molecule neuroligin-4 were repeatedly identified as monogenetic causes of autism. In mice, neuroligin-4 deletions caused autism-related behavioral impairments and subtle changes in synaptic transmission, and neuroligin-4 was found, at least in part, at glycinergic synapses. However, low expression levels precluded a comprehensive analysis of neuroligin-4 localization, and overexpression of neuroligin-4 puzzlingly impaired excitatory but not inhibitory synaptic function. As a result, the function of neuroligin-4 remains unclear, as does its relation to other neuroligins. To clarify these issues, we systematically examined the function of neuroligin-4, focusing on excitatory and inhibitory inputs to defined projection neurons of the mouse brainstem as central model synapses. We show that loss of neuroligin-4 causes a profound impairment of glycinergic but not glutamatergic synaptic transmission and a decrease in glycinergic synapse numbers. Thus, neuroligin-4 is essential for the organization and/or maintenance of glycinergic synapses.
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Registered trials
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