ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Abnormal presynaptic short-term plasticity and information processing in a mouse model of fragile X syndrome.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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96 citing papers in PubMed.
- Stimulation of the medial septum diagonal band of broca rescues learning and memory deficits iniScience · 2026Article
- Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools.Cell reports · 2026Article
- Dysfunctional neural dynamics associated with sensory phenotypes in Fragile X syndrome: insights from mouse models.Journal of neurodevelopmental disorders · 2025Review
- Disrupted theta synchronization and synaptic connectivity in the visual cortex of Fmr1 KO mice.Nature communications · 2025Article
- Aberrant hippocampal gamma oscillations in a mouse model of fragile X syndrome: insights from in vitro slice models.Molecular autism · 2025Article
- Frequency-Dependent Modulation of Short-Term Neuronal Dynamics in the Female and Male Dorsal and Ventral Rat Hippocampus.International journal of molecular sciences · 2025Article
- Region-Related Differences in Short-Term Synaptic Plasticity and Synaptotagmin-7 in the Male and Female Hippocampus of a Rat Model of Fragile X Syndrome.International journal of molecular sciences · 2024Article
- Assessment of the excitation-inhibition ratio in the Fmr1 KO2 mouse using neuronal oscillation dynamics.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Oligodendrocyte-derived LGI3 and its receptor ADAM23 organize juxtaparanodal Kv1 channel clustering for short-term synaptic plasticity.Cell reports · 2024Article
- Large conductance voltage-and calcium-activated KFrontiers in pharmacology · 2024Review
- Septotemporal Variation of Information Processing in the Hippocampus of Fmr1 KO Rat.Developmental neuroscience · 2024Article
- The activation of mGluR4 rescues parallel fiber synaptic transmission and LTP, motor learning and social behavior in a mouse model of Fragile X Syndrome.Molecular autism · 2023Article
- Axonal and presynaptic FMRP: Localization, signal, and functional implications.Hearing research · 2023Review
- Cellular distribution of the Fragile X mental retardation protein in the inner ear: a developmental and comparative study in the mouse, rat, gerbil, and chicken.The Journal of comparative neurology · 2023Article
- FMRP activity and control of Csw/SHP2 translation regulate MAPK-dependent synaptic transmission.PLoS biology · 2023Article
- Review
- Article
- Keeping Excitation-Inhibition Ratio in Balance.International journal of molecular sciences · 2022Review
- Multiscale modeling of presynaptic dynamics from molecular to mesoscale.PLoS computational biology · 2022Article
- FMRP Sustains Presynaptic Function via Control of Activity-Dependent Bulk Endocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
36 more citing papers are in PubMed but not listed here.
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3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Fragile X syndrome (FXS) is the most common inherited form of intellectual disability and the leading genetic cause of autism. It is associated with the lack of fragile X mental retardation protein (FMRP), a regulator of protein synthesis in axons and dendrites. Studies on FXS have extensively focused on the postsynaptic changes underlying dysfunctions in long-term plasticity. In contrast, the presynaptic mechanisms of FXS have garnered relatively little attention and are poorly understood. Activity-dependent presynaptic processes give rise to several forms of short-term plasticity (STP), which is believed to control some of essential neural functions, including information processing, working memory, and decision making. The extent of STP defects and their contributions to the pathophysiology of FXS remain essentially unknown, however. Here we report marked presynaptic abnormalities at excitatory hippocampal synapses in Fmr1 knock-out (KO) mice leading to defects in STP and information processing. Loss of FMRP led to enhanced responses to high-frequency stimulation. Fmr1 KO mice also exhibited abnormal synaptic processing of natural stimulus trains, specifically excessive enhancement during the high-frequency spike discharges associated with hippocampal place fields. Analysis of individual STP components revealed strongly increased augmentation and reduced short-term depression attributable to loss of FMRP. These changes were associated with exaggerated calcium influx in presynaptic neurons during high-frequency stimulation, enhanced synaptic vesicle recycling, and enlarged readily-releasable and reserved vesicle pools. These data suggest that loss of FMRP causes abnormal STP and information processing, which may represent a novel mechanism contributing to cognitive impairments in FXS.
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