ArticlePloS one2013
Asymmetric N-cadherin expression results in synapse dysfunction, synapse elimination, and axon retraction in cultured mouse neurons.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Adherent junctions: Physiology, role in hydrocephalus and potential therapeutic targets.IBRO neuroscience reports · 2025Review
- Plk2 promotes synaptic destabilization through disruption of N-cadherin adhesion complexes during homeostatic adaptation to hyperexcitation.Journal of neurochemistry · 2023Article
- Proteomics of the dentate gyrus reveals semantic dementia specific molecular pathology.Acta neuropathologica communications · 2022Article
- Flying under the radar: CDH2 (N-cadherin), an important hub molecule in neurodevelopmental and neurodegenerative diseases.Frontiers in neuroscience · 2022Review
- CDH2 mutation affecting N-cadherin function causes attention-deficit hyperactivity disorder in humans and mice.Nature communications · 2021Article
- Review
- Levetiracetam and N-Cadherin Antibody Alleviate Brain Pathology Without Reducing Early Epilepsy Development After Focal Non-convulsive Status Epilepticus in Rats.Frontiers in neurology · 2021Article
- Urokinase-Type Plasminogen Activator Protects Cerebral Cortical Neurons from Soluble Aβ-Induced Synaptic Damage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Spinal N-Cadherin/CREB Signaling Contributes to Chronic Alcohol Consumption-Enhanced Postsurgical Pain.Journal of pain research · 2020Article
- Differential Properties of the Synaptogenic Activities of the Neurexin Ligands Neuroligin1 and LRRTM2.Frontiers in molecular neuroscience · 2019Article
- Long-term depression-associated signaling is required for an in vitro model of NMDA receptor-dependent synapse pruning.Neurobiology of learning and memory · 2017Article
- Release activity-dependent control of vesicle endocytosis by the synaptic adhesion molecule N-cadherin.Scientific reports · 2017Article
- Properties of Retinal Precursor Cells Grown on Vertically Aligned Multiwalled Carbon Nanotubes Generated for the Modification of Retinal Implant-Embedded Microelectrode Arrays.Journal of ophthalmology · 2016Article
- Learning From Animal Models of Obsessive-Compulsive Disorder.Biological psychiatry · 2016Review
- δ-Catenin Regulates Spine Architecture via Cadherin and PDZ-dependent Interactions.The Journal of biological chemistry · 2015Article
- Alzheimer's disease-related amyloid-β induces synaptotoxicity in human iPS cell-derived neurons.Cell death & disease · 2015Article
- N-cadherin participated in invasion and metastasis of human esophageal squamous cell carcinoma via taking part in the formation of vasculogenic mimicry.Medical oncology (Northwood, London, England) · 2015Article
- Cadherins and catenins in dendrite and synapse morphogenesis.Cell adhesion & migration · 2015Review
- Cadherin-based transsynaptic networks in establishing and modifying neural connectivity.Current topics in developmental biology · 2015Review
- N-cadherin regulates molecular organization of excitatory and inhibitory synaptic circuits in adult hippocampus in vivo.Hippocampus · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synapse elimination and pruning of axon collaterals are crucial developmental events in the refinement of neuronal circuits. While a control of synapse formation by adhesion molecules is well established, the involvement of adhesion molecules in developmental synapse loss is poorly characterized. To investigate the consequences of mis-match expression of a homophilic synaptic adhesion molecule, we analysed an asymmetric, exclusively postsynaptic expression of N-cadherin. This was induced by transfecting individual neurons in cultures of N-cadherin knockout mouse neurons with a N-cadherin expression vector. 2 days after transfection, patch-clamp analysis of AMPA receptor-mediated miniature postsynaptic currents revealed an impaired synaptic function without a reduction in the number of presynaptic vesicle clusters. Long-term asymmetric expression of N-cadherin for 8 days subsequently led to synapse elimination as indicated by a loss of colocalization of presynaptic vesicles and postsynaptic PSD95 protein. We further studied long-term asymmetric N-cadherin expression by conditional, Cre-induced knockout of N-cadherin in individual neurons in cultures of N-cadherin expressing cortical mouse neurons. This resulted in a strong retraction of axonal processes in individual neurons that lacked N-cadherin protein. Moreover, an in vivo asymmetric expression of N-cadherin in the developmentally transient cortico-tectal projection was indicated by in-situ hybridization with layer V neurons lacking N-cadherin expression. Thus, mis-match expression of N-cadherin might contribute to selective synaptic connectivity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.