Altered synaptic plasticity in a mouse model of fragile X mental retardation

By K. Huber, Sean M Gallagher, S. Warren, Mark F. Bear. Proceedings of the National Academy of Sciences of the United States of America, 2002

1,322 citations recorded by the source corpus.

Subfields: Cell Biology, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/15019fa1055c3670daa3e4410fa25691863b0692

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Citations in the corpus

The autistic neuron: troubled translation? (2008, background): “Interestingly, mGluR-dependent LTD, which requires translation but not transcription for its expression, is significantly enhanced in the hippocampus of Fmr1 knockout mice (Huber et al., 2002).”
Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms (2008, background): “This link between protein synthesis and mGluR LTD gained considerable attention following the report that mice lacking the gene encoding the fragile X mental retardation protein (FMRP) exhibited enhanced mGluR LTD in both the hippocampus (Huber et al, 2002) and the cerebellum (Koekkoek et al, 2005).”
Fragile X Mental Retardation Protein: A Paradigm for Translational Control by RNA-Binding Proteins (2015, result): “Consistent with the mGluR hypothesis, studies indicate that LTD is exaggerated in Fmr1 KO mice and does not require new protein synthesis (Huber et al., 2002; Nosyreva and Huber, 2006).”
Dendritic mRNA: transport, translation and function (2007, background): “Consistent with this idea, loss of FMRP results in an enhancement of LTD amplitud”
Biochemical and genetic interaction between the fragile X mental retardation protein and the microRNA pathway (2004, background): “Consistent with this model, the long-term depression (LTD) that depends on protein synthesis and is triggered by activation of metabotropic glutamate receptors is markedly increased in the hippocampus of Fmr1 knockout mic”
Long-term depression in the CNS (2010, background): “Interestingly, mGluR-LTD(A) is facilitated in mice that lack the gene encoding fragile X mental retardation protein ( FMRP”
Translational control of long-lasting synaptic plasticity and memory. (2009, positive): “Interestingly, in FMRP knockout mice, mGluR- LTD is enhanced and no longer requires protein synthesis (Hou et al., 2006; Huber et al., 2002; Nosyreva and Huber, 2006).”
The fragile X syndrome protein represses activity-dependent translation through CYFIP1, a new 4E-BP. (2008, methodology): “**p < 0.01, *p < 0.05, Student’s t test. caused CYFIP1-eIF4E dissociation (Figure 6D), confirming a response of FMRP translational repression to mGluR signaling (Huber et al., 2002; Hou et al., 2006; Dolen et al., 2007).”
Metabotropic glutamate receptors: From the workbench to the bedside (2010, background): “Remarkably, other forms of synaptic plasticity, including the more classical NMDA-receptor dependent LTD, showno abnormalities in the hippocampus of Fmr1 knockout mice (Huber et al., 2002; reviewed by Waung and Huber, 2009).”
Metaplasticity: tuning synapses and networks for plasticity (2008, neutral): “cgi?id=300624">Fragile X-linked mental retardation syndrome”
Correction of fragile X syndrome in mice. (2007, background): “…mGluR1 and mGluR5 (Weiler and Greenough, 1993); (3) many of the lasting consequences of activating Gp1 mGluRs depend on synaptic mRNA translation (Huber et al., 2000; Karachot et al., 2001; Merlin et al., 1998; Raymond et al., 2000; Vanderklish and Edelman, 2002; Zho et al., 2002); and (4)…”
Normal Development of Brain Circuits (2010, background): “In Fragile X syndrome, the most common genetic cause of mental retardation, silencing of the Fmr1 gene (Devys et al, 1992) seems to disrupt the balance between long-term potentiation and depression (Bagni and Greenough, 2005; Huber et al, 2002).”
The mGluR theory of fragile X mental retardation. (2004, positive): “Fmr1 knockout mouse suggested a novel connection between metabotropic glutamate receptor (mGluR) signaling and the fragile X phenotype [ 13 ].”