ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Restoration of synaptic plasticity and learning in young and aged NCAM-deficient mice by enhancing neurotransmission mediated by GluN2A-containing NMDA receptors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 48 citations in OpenAlex.
- Sleep-dependent declarative memory consolidation--unaffected after blocking NMDA or AMPA receptors but enhanced by NMDA coagonist D-cycloserine.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2013Trial
- Polysialic Acid Modulation of Glutamate Receptors and Synaptic Mechanisms Underlying Neuronal Plasticity.NeuroSci · 2026Review
- Cell-autonomous GABAARs are essential for NMDAR-mediated synaptic transmission, LTP, and spatial memory.EMBO reports · 2025Article
- Neural ageing and synaptic plasticity: prioritizing brain health in healthy longevity.Frontiers in aging neuroscience · 2024Review
- Synaptic cell adhesion molecules contribute to the pathogenesis and progression of fragile X syndrome.Frontiers in cellular neuroscience · 2024Review
- Article
- The Application of the Neuroprotective and Potential Antioxidant Effect of Ergotamine Mediated by Targeting N-Methyl-D-Aspartate Receptors.Antioxidants (Basel, Switzerland) · 2022Article
- Sialometabolism in Brain Health and Alzheimer's Disease.Frontiers in neuroscience · 2021Review
- Amygdala GluN2B-NMDAR dysfunction is critical in abnormal aggression of neurodevelopmental origin induced by St8sia2 deficiency.Molecular psychiatry · 2020Article
- New Treatment Strategies of Depression: Based on Mechanisms Related to Neuroplasticity.Neural plasticity · 2017Review
- Environmental Enrichment Ameliorates Behavioral Impairments Modeling Schizophrenia in Mice Lacking Metabotropic Glutamate Receptor 5.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Article
- Activity dependent CAM cleavage and neurotransmission.Frontiers in cellular neuroscience · 2015Review
- NMDA Receptor Function During Senescence: Implication on Cognitive Performance.Frontiers in neuroscience · 2015Review
- Sialic acids in the brain: gangliosides and polysialic acid in nervous system development, stability, disease, and regeneration.Physiological reviews · 2014Review
- A role for hippocampal PSA-NCAM and NMDA-NR2B receptor function in flavonoid-induced spatial memory improvements in young rats.Neuropharmacology · 2014Article
- Tegaserod mimics the neurostimulatory glycan polysialic acid and promotes nervous system repair.Neuropharmacology · 2014Article
- The impact of the genome-wide supported variant in the cyclin M2 gene on gray matter morphology in schizophrenia.Behavioral and brain functions : BBF · 2013Article
- Dynein interacts with the neural cell adhesion molecule (NCAM180) to tether dynamic microtubules and maintain synaptic density in cortical neurons.The Journal of biological chemistry · 2013Article
- Depletion of polysialic acid from neural cell adhesion molecule (PSA-NCAM) increases CA3 dendritic arborization and increases vulnerability to excitotoxicity.Experimental neurology · 2013Article
- Functional role of the interaction between polysialic acid and myristoylated alanine-rich C kinase substrate at the plasma membrane.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 4 countries.
Funding
Abstract
Neural cell adhesion molecule (NCAM) is the predominant carrier of the unusual glycan polysialic acid (PSA). Deficits in PSA and/or NCAM expression cause impairments in hippocampal long-term potentiation and depression (LTP and LTD) and are associated with schizophrenia and aging. In this study, we show that impaired LTP in adult NCAM-deficient (NCAM(-/-)) mice is restored by increasing the activity of the NMDA subtype of glutamate receptor (GluN) through either reducing the extracellular Mg2+ concentration or applying d-cycloserine (DCS), a partial agonist of the GluN glycine binding site. Pharmacological inhibition of the GluN2A subtype reduced LTP to the same level in NCAM(-/-) and wild-type (NCAM(+/+)) littermate mice and abolished the rescue by DCS in NCAM(-/-) mice, suggesting that the effects of DCS are mainly mediated by GluN2A. The insufficient contribution of GluN to LTD in NCAM(-/-) mice was also compensated for by DCS. Furthermore, impaired contextual and cued fear conditioning levels were restored in NCAM(-/-) mice by administration of DCS before conditioning. In 12-month-old NCAM(-/-), but not NCAM(+/+) mice, there was a decline in LTP compared with 3-month-old mice that could be rescued by DCS. In 24-month-old mice of both genotypes, there was a reduction in LTP that could be fully restored by DCS in NCAM(+/+) mice but only partially restored in NCAM(-/-) mice. Thus, several deficiencies of NCAM(-/-) mice can be ameliorated by enhancing GluN2A-mediated neurotransmission with DCS.
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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.