Neuroligins determine synapse maturation and function.

By F. Varoqueaux, G. Aramuni, Randi L. Rawson, R. Mohrmann, M. Missler, K. Gottmann, Weiqi Zhang, T. Sūdhof, N. Brose. Neuron, 2006

819 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience

View Paper: https://www.semanticscholar.org/paper/a2bb60f58b8a31d11730bd97d7a8643a73a1b2f0

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

In Developmental Neuroscience

Citations in the corpus

Modelling learning and memory in Drosophila to understand Intellectual Disabilities. (2020, neutral): “Neurexin and their binding partners, the neuroligins, are central organizing molecules at synapses that work as adhesion proteins and regulate pre- and post- synapse maturation and activity (Scheiffele et al., 2000; Graf et al., 2004; Varoqueaux et al., 2006; Südhof, 2017).”
Neurexin-neuroligin signaling in synapse development. (2007, background): “This is a daunting task in mammals, but it has been addressed heroically by generation and analysis of Nrxn1;Nrxn2;Nrxn3 triple mutant mice that lack all three a-neurexins [46] and of Nlgn1;Nlgn2;Nlgn3 triple neuroligin knockout mice [47 ].”
Activity-dependent validation of excitatory versus inhibitory synapses by neuroligin-1 versus neuroligin-2. (2007, neutral): “Indeed, results from knockout (KO) mice demonstrated that neither NLs nor a-neurexins are required for the initial formation of synapses, but both are essential for synaptic function and mouse survival (Missler et al., 2003; Varoqueaux et al., 2006).”
GFP Reconstitution Across Synaptic Partners (GRASP) defines cell contacts and synapses in living nervous systems. (2008, background): “In the vertebrate central nervous system, neuroligins are preferentially localized to postsynaptic sites, where they interact with presynaptic neurexins to affect synaptic maturation and func- tion (Craig and Kang, 2007; Varoqueaux et al., 2006).”
Neuroligins and neurexins link synaptic function to cognitive disease (2008, background): “I suggest that these molecules are required for synapse function but not for synapse formation, that they affect trans-synaptic activation of synaptic transmission but are not essential for synaptic cohesion of the presynaptic and postsynaptic specializations, and that their dysfunction impairs the ”
Mapping autism risk loci using genetic linkage and chromosomal rearrangements (2007, background): “Called CNVs were also examined for overlap with genomic features including mapped chromosome rearrangement breakpoints annotated in the Autism Chromo-some Rearrangement Database and polymorphic CNVs in the Database of Genomic Variants.”
Cell adhesion molecules: signalling functions at the synapse (2007, background): “Mice lacking neuroligins 1–3 die shortly after birth due to respiratory failur”
Synaptic dysfunction in neurodevelopmental disorders associated with autism and intellectual disabilities. (2012, background): “Neurophysiological studies revealed that glutamatergic and GABAergic/glycinergic synaptic transmission is impaired in the respiratory centers of the triple null animals (Varoqueaux et al. 2006).”
Neuronal Activity Promotes Glioma Growth through Neuroligin-3 Secretion (2015, neutral): “The neuroligins are post-synaptic adhesion molecules that are important in synaptic function and plasticity (Südhof, 2008; Varoqueaux et al., 2006).”