ArticleFrontiers in synaptic neuroscience2015
Genetic targeting of NRXN2 in mice unveils role in excitatory cortical synapse function and social behaviors.
Article in Frontiers in synaptic neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Neurexin dysfunction in neurodevelopmental and neuropsychiatric disorders: a PRIMSA-based systematic review through iPSC and animal models.Frontiers in behavioral neuroscience · 2024Pooled it
- Signaling Through Girdin Underlies Excessive Cell Morphogenesis Resulting from Depletion of Neurodevelopmental Disorder-Related Neurexin-2.International journal of molecular sciences · 2026Article
- Distinct and combined interferon-ɑ/β-receptor-1 loss in neurons and astrocytes disrupt brain energy metabolism and drive Parkinsonian dementia.Journal of biomedical science · 2026Article
- Roles of synaptic cell adhesion molecules in the neuromodulatory systems.Molecules and cells · 2026Review
- Autism Spectrum Disorder: The Cerebellum, Genes, and Pathways.Neurology international · 2025Review
- Abnormal O-glycan sialylation in the mPFC contributes to depressive-like behaviors in male mice.Science advances · 2025Article
- Perturbed synaptic adhesion molecules signaling in neurodevelopmental disorders: The impact of metal neurotoxicity.Ibrain · 2025Review
- Alpha-neurexins in health and disease.Frontiers in molecular neuroscience · 2025Review
- Conserved autism-associated genes tune social feeding behavior in C. elegans.Nature communications · 2024Article
- Conditional deletion of neurexin-2 impaired behavioral flexibility to alterations in action-outcome contingency.Scientific reports · 2024Article
- Structural and functional characterization of the IgSF21-neurexin2α complex and its related signaling pathways in the regulation of inhibitory synapse organization.Frontiers in molecular neuroscience · 2024Article
- Conserved autism-associated genes tune social feeding behavior inbioRxiv : the preprint server for biology · 2023Article
- Distinct neurexin isoforms cooperate to initiate and maintain foraging activity.Translational psychiatry · 2023Article
- Clinical and Osteopetrosis-Like Radiological Findings in Patients with Leukocyte Adhesion Deficiency Type III.Journal of clinical immunology · 2023Article
- Case Report-An Inherited Loss-of-FunctionGenes · 2023Article
- Critical periods and Autism Spectrum Disorders, a role for sleep.Neurobiology of sleep and circadian rhythms · 2023Article
- α-Synuclein Preformed Fibrils Bind to β-Neurexins and Impair β-Neurexin-Mediated Presynaptic Organization.Cells · 2023Article
- Neurexin-2 restricts synapse numbers and restrains the presynaptic release probability by an alternative splicing-dependent mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Conditional deletion of Neurexin-2 alters neuronal network activity in hippocampal circuitries and leads to spontaneous seizures.Translational psychiatry · 2023Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human genetics has identified rare copy number variations and deleterious mutations for all neurexin genes (NRXN1-3) in patients with neurodevelopmental diseases, and electrophysiological recordings in animal brains have shown that Nrxns are important for synaptic transmission. While several mouse models for Nrxn1α inactivation have previously been studied for behavioral changes, very little information is available for other variants. Here, we validate that mice lacking Nrxn2α exhibit behavioral abnormalities, characterized by social interaction deficits and increased anxiety-like behavior, which partially overlap, partially differ from Nrxn1α mutant behaviors. Using patch-clamp recordings in Nrxn2α knockout brains, we observe reduced spontaneous transmitter release at excitatory synapses in the neocortex. We also analyse at this cellular level a novel NRXN2 mouse model that carries a combined deletion of Nrxn2α and Nrxn2β. Electrophysiological analysis of this Nrxn2-mutant mouse shows surprisingly similar defects of excitatory release to Nrxn2α, indicating that the β-variant of Nrxn2 has no strong function in basic transmission at these synapses. Inhibitory transmission as well as synapse densities and ultrastructure remain unchanged in the neocortex of both models. Furthermore, at Nrxn2α and Nrxn2-mutant excitatory synapses we find an altered facilitation and N-methyl-D-aspartate receptor (NMDAR) function because NMDAR-dependent decay time and NMDAR-mediated responses are reduced. As Nrxn can indirectly be linked to NMDAR via neuroligin and PSD-95, the trans-synaptic nature of this complex may help to explain occurrence of presynaptic and postsynaptic effects. Since excitatory/inhibitory imbalances and impairment of NMDAR function are alledged to have a role in autism and schizophrenia, our results support the idea of a related pathomechanism in these disorders.
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