ArticleFrontiers in psychiatry2019
Possible Implication of the CA2 Hippocampal Circuit in Social Cognition Deficits Observed in the Neuroligin 3 Knock-Out Mouse, a Non-Syndromic Animal Model of Autism.
Article in Frontiers in psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 54 citations in OpenAlex.
- Neuroligin1 in CCK-interneurons gates social memory formation via a disinhibitory microcircuit in the hippocampal CA2 in male mice.Nature communications · 2026Article
- Convergent depression of activity-dependent bulk endocytosis in rodent models of autism spectrum disorder.Molecular autism · 2025Article
- Sleepless nights and social plights: medial septum GABAergic hyperactivity in a neuroligin 3-deficient autism model.The Journal of clinical investigation · 2024Article
- Autism-associated neuroligin 3 deficiency in medial septum causes social deficits and sleep loss in mice.The Journal of clinical investigation · 2024Article
- Identification of hippocampal area CA2 in hamster and vole brain.The Journal of comparative neurology · 2024Article
- Identification of hippocampal area CA2 in hamster and vole brain.bioRxiv : the preprint server for biology · 2024Article
- Functional connectivity of the sensorimotor cerebellum in autism: associations with sensory over-responsivity.Frontiers in psychiatry · 2024Article
- Insights into the structure and function of the hippocampus: implications for the pathophysiology and treatment of autism spectrum disorder.Frontiers in psychiatry · 2024Review
- Unraveling the Role of Neuroligin3 in Autism Spectrum Disorders: Pathophysiological Insights and Targeted Therapies.CNS & neurological disorders drug targets · 2024Review
- Reduced Cholecystokinin-Expressing Interneuron Input Contributes to Disinhibition of the Hippocampal CA2 Region in a Mouse Model of Temporal Lobe Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Article
- Activation of the CA2-ventral CA1 pathway reverses social discrimination dysfunction in Shank3B knockout mice.Nature communications · 2023Article
- Impaired synaptic plasticity in an animal model of autism exhibiting early hippocampal GABAergic-BDNF/TrkB signaling alterations.iScience · 2023Article
- The little brain and the seahorse: Cerebellar-hippocampal interactions.Frontiers in systems neuroscience · 2023Review
- Hippocampal area CA2: interneuron disfunction during pathological states.Frontiers in neural circuits · 2023Review
- Machine learning-based segmentation of the rodent hippocampal CA2 area from Nissl-stained sections.Frontiers in neuroanatomy · 2023Article
- Insulin-like growth factor 2 (IGF-2) rescues social deficits in NLG3Frontiers in cellular neuroscience · 2023Article
- Imbalance of flight-freeze responses and their cellular correlates in the Nlgn3Molecular autism · 2022Article
- Neuroligins in neurodevelopmental conditions: how mouse models ofNeuronal signaling · 2022Article
- Neuroligin-3 Regulates Excitatory Synaptic Transmission and EPSP-Spike Coupling in the Dentate Gyrus In Vivo.Molecular neurobiology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorders (ASDs) comprise a heterogeneous group of neuro-developmental abnormalities with a strong genetic component, characterized by deficits in verbal and non-verbal communication, impaired social interactions, and stereotyped behaviors. In a small percentage of cases, ASDs are associated with alterations of genes involved in synaptic function. Among these, relatively frequent are mutations/deletions of genes encoding for neuroligins (NLGs). NLGs are postsynaptic adhesion molecules that, interacting with their presynaptic partners neurexins, ensure the cross talk between pre- and postsynaptic specializations and synaptic stabilization, a condition needed for maintaining a proper excitatory/inhibitory balance within local neuronal circuits. We have focused on mice lacking NLG3 (NLG3 knock-out mice), animal models of a non-syndromic form of autism, which exhibit deficits in social behavior reminiscent of those found in ASDs. Among different brain areas involved in social cognition, the CA2 region of the hippocampus has recently emerged as a central structure for social memory processing. Here,
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