Neurexin Dysfunction in Adult Neurons Results in Autistic-like Behavior in Mice
Open accessAbstract
Autism spectrum disorders (ASDs) comprise a group of clinical phenotypes characterized by repetitive behavior and social and communication deficits. Autism is generally viewed as a neurodevelopmental disorder where insults during embryonic or early postnatal periods result in aberrant wiring and function of neuronal circuits. Neurexins are synaptic proteins associated with autism. Here, we generated transgenic βNrx1ΔC mice in which neurexin function is selectively impaired during late postnatal stages. Whole-cell recordings in cortical neurons show an impairment of glutamatergic synaptic transmission in the βNrx1ΔC mice. Importantly, mutant mice exhibit autism-related symptoms, such as increased self-grooming, deficits in social interactions, and altered interaction for nonsocial olfactory cues. The autistic-like phenotype of βNrx1ΔC mice can be reversed after removing the mutant protein in aged animals. The defects resulting from disruption of neurexin function after the completion of embryonic and early postnatal development suggest that functional impairment of mature circuits can trigger autism-related phenotypes.
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In mice, only mild phenotypes and varying results have been described in the social spectrum after nrxn1 ablation.
“but in the social spectrum, only mild phenotypes and varying results have been described (Grayton et al. 2013, Rabaneda et al. 2014, Dachtler et al. 2015; Armstrong et al. 2020).”
From Neurexin1α knockout in rats causes aberrant social behaviour: relevance for autism and schizophrenia (2025) · cites this paper as Rabaneda et al. 2014
The ‘Autistic-like Behavior of bNrx1DC Mice’ section reports social deficits in both young and aged mice, including reduced interaction with a novel mouse; the Discussion also describes defects in sociability and social preference. Rather than reporting only mild or varying social findings after nrxn1 ablation, this paper studies mice expressing a mutant neurexin-1b protein and reports deficits replicated across ages. (LLM, conf=0.85)
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Cites
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Sex Hormones Regulate SHANK Expression
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Neurexin1α knockout in rats causes aberrant social behaviour: relevance for autism and schizophrenia
Achterberg, E. J. M., Biemans, B., & Vanderschuren, L. J. M. J. (2025) · Psychopharmacology · doi:10.1007/s00213-024-06559-z · Cited by 9 · see citing works
“…inhibition and spatial memory, and increased grooming and motor learning (Etherton et al. 2009; Blundell et al. 2010), but in the social spectrum, only mild phenotypes and varying results have been described (Grayton et al. 2013, Rabaneda et al. 2014, Dachtler et al. 2015; Armstrong et al. 2020).”
- Authors
- Rabaneda, L. G., Robles-Lanuza, E., Nieto-González, J. L., & Scholl, F. G.
- Affiliations
- Consejo Superior de Investigaciones Científicas (ES)
- Corresponding author
- Scholl, Francisco G.
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2014-07
- Volume
- 8
- Issue
- 2
- Pages
- 338-346
- ISSN
- 2211-1247 (ISSN-L)
- OpenAlex
- W2054725419
- Cited by
- 78
- References
- 10
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 4 · 2023: 3 · 2022: 4 · 2021: 8 · 2020: 10 · 2019: 6 · 2018: 7 · 2017: 11 · 2016: 8 · 2015: 9
- FWCI
- 6.12
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Deposito de Investigacion Universidad de Sevilla (University of Seville) (submittedVersion, cc-by-nc-nd)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- neurexin, NRXN1, autism spectrum disorder, adult neurons, glutamatergic neurotransmission, cortical neurons, social interaction deficits, self-grooming, olfactory interaction, postnatal development, synaptic proteins, autism-like behavior
- MeSH terms
- Animals, Autistic Disorder, Calcium-Binding Proteins, Cells, Cultured, Cerebral Cortex, Grooming, Mutation, Neurons, Phenotype, Social Behavior, Neural Cell Adhesion Molecules, Mice, Inhibitory Postsynaptic Potentials
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