ArticleNeuroscience2012
Synaptic NMDA receptor-mediated currents in anterior piriform cortex are reduced in the adult fragile X mouse.
Article in Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Neonatal expression of human FMRP isoform corrects cortical deficits and improves behavior in a mouse model of fragile X syndrome.Molecular therapy. Nucleic acids · 2026Article
- Olfactory dysfunction and altered cortical excitability in the mouse model of Fragile X Syndrome.Biological research · 2025Article
- Anterior piriform cortex dysfunction underlies autism spectrum disorders-related olfactory deficits in Fmr1 conditional deletion mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Therapeutic Effects of Pharmacological Modulation of Serotonin Brain System in Human Patients and Animal Models of Fragile X Syndrome.International journal of molecular sciences · 2025Review
- Axonal and presynaptic FMRP: Localization, signal, and functional implications.Hearing research · 2023Review
- Spaced training improves learning in Ts65Dn and Ube3a mouse models of intellectual disabilities.Translational psychiatry · 2019Article
- Pituitary Adenylate Cyclase-Activating Polypeptide Modulates Hippocampal Synaptic Transmission and Plasticity: New Therapeutic Suggestions for Fragile X Syndrome.Frontiers in cellular neuroscience · 2019Review
- Sumoylation regulates FMRP-mediated dendritic spine elimination and maturation.Nature communications · 2018Article
- Relationship Between Synaptic AMPAR and Spine Dynamics: Impairments in the FXS Mouse.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- Synaptic Plasticity, a Prominent Contributor to the Anxiety in Fragile X Syndrome.Neural plasticity · 2016Review
- Functional and structural deficits at accumbens synapses in a mouse model of Fragile X.Frontiers in cellular neuroscience · 2015Article
- Targeted pharmacological treatment of autism spectrum disorders: fragile X and Rett syndromes.Frontiers in cellular neuroscience · 2015Review
- The role of ionotropic glutamate receptors in childhood neurodevelopmental disorders: autism spectrum disorders and fragile x syndrome.Current neuropharmacology · 2014Article
- Evidence for loss of synaptic AMPA receptors in anterior piriform cortex of aged mice.Frontiers in aging neuroscience · 2013Article
- Hyperactivity, perseveration and increased responding during attentional rule acquisition in the Fragile X mouse model.Frontiers in behavioral neuroscience · 2013Article
- Group 1 metabotropic glutamate receptor function and its regulation of learning and memory in the aging brain.Frontiers in pharmacology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Fragile X syndrome is a neurodevelopmental condition caused by the transcriptional silencing of the fragile X mental retardation 1 (FMR1) gene. The Fmr1 knockout (KO) mouse exhibits age-dependent deficits in long term potentiation (LTP) at association (ASSN) synapses in anterior piriform cortex (APC). To investigate the mechanisms for this, whole-cell voltage-clamp recordings of ASSN stimulation-evoked synaptic currents were made in APC of slices from adult Fmr1-KO and wild-type (WT) mice, using the competitive N-methyl-D-aspartate (NMDA) receptor antagonist, CPP, to distinguish currents mediated by NMDA and AMPA receptors. NMDA/AMPA current ratios were lower in Fmr1-KO mice than in WT mice, at ages ranging from 3-18months. Since amplitude and frequency of miniature excitatory postsynaptic currents (mEPSCs) mediated by AMPA receptors were no different in Fmr1-KO and WT mice at these ages, the results suggest that NMDA receptor-mediated currents are selectively reduced in Fmr1-KO mice. Analyses of voltage-dependence and decay kinetics of NMDA receptor-mediated currents did not reveal differences between Fmr1-KO and WT mice, suggesting that reduced NMDA currents in Fmr1-KO mice are due to fewer synaptic receptors rather than differences in receptor subunit composition. Reduced NMDA receptor signaling may help to explain the LTP deficit seen at APC ASSN synapses in Fmr1-KO mice at 6-18months of age, but does not explain normal LTP at these synapses in mice 3-6months old. Evoked currents and mEPSCs were also examined in senescent Fmr1-KO and WT mice at 24-28months of age. NMDA/AMPA ratios were similar in senescent WT and Fmr1-KO mice, due to a decrease in the ratio in the WT mice, without significant change in AMPA receptor-mediated mEPSCs.
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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.