The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.
Ras Signaling Mechanisms Underlying Impaired GluR1-Dependent Plasticity Associated with Fragile X Syndrome
Open accessAbstract
Fragile X syndrome, caused by the loss of FMR1 gene function and loss of fragile X mental retardation protein (FMRP), is the most commonly inherited form of mental retardation. The syndrome is characterized by associative learning deficits, reduced risk of cancer, dendritic spine dysmorphogenesis, and facial dysmorphism. However, the molecular mechanism that links loss of function of FMR1 to the learning disability remains unclear. Here, we report an examination of small GTPase Ras signaling and synaptic AMPA receptor (AMPA-R) trafficking in cultured slices and intact brains of wild-type and FMR1 knock-out mice. In FMR1 knock-out mice, synaptic delivery of GluR1-, but not GluR2L- and GluR4-containing AMPA-Rs is impaired, resulting in a selective loss of GluR1-dependent long-term synaptic potentiation (LTP). Although Ras activity is upregulated, its downstream MEK (extracellular signal-regulated kinase kinase)–ERK (extracellular signal-regulated kinase) signaling appears normal, and phosphoinositide 3-kinase (PI3K)–protein kinase B (PKB; or Akt) signaling is compromised in FMR1 knock-out mice. Enhancing Ras–PI3K–PKB signaling restores synaptic delivery of GluR1-containing AMPA-Rs and normal LTP in FMR1 knock-out mice. These results suggest aberrant Ras signaling as a novel mechanism for fragile X syndrome and indicate manipulating Ras–PI3K–PKB signaling to be a potentially effective approach for treating patients with fragile X syndrome.
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Cites
AKT/PKB signaling: navigating downstream
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AMPA Receptor Trafficking and Synaptic Plasticity
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Abnormal dendritic spines in fragile X knockout mice: Maturation and pruning deficits
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The role of the GluR2 subunit in AMPA receptor function and synaptic plasticity
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Importance of AMPA Receptors for Hippocampal Synaptic Plasticity But Not for Spatial Learning
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Subunit-specific temporal and spatial patterns of AMPA receptor exocytosis in hippocampal neurons
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Abnormal Development of Dendritic Spines in FMR1 Knock-Out Mice
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Cited by
Bidirectional control of social hierarchy by synaptic efficacy in medial prefrontal cortex
Wang, F., Zhu, J., Zhu, H., Zhang, Q., Lin, Z., & Hu, H. (2011) · Science · doi:10.1126/science.1209951 · Cited by 528
Self-citationHazlett, H. C., Poe, M. D., Gerig, G., Styner, M., Chappell, C., Smith, R. G., Vachet, C., & Piven, J. (2011) · Archives of General Psychiatry · doi:10.1001/archgenpsychiatry.2011.39 · Cited by 481
Dendritic Spines: The Locus of Structural and Functional Plasticity
Sala, C., & Segal, M. (2014) · Physiological Reviews · doi:10.1152/physrev.00012.2013 · Cited by 465
The Pathophysiology of Fragile X (and What It Teaches Us about Synapses)
Bhakar, A. L., Dölen, G., & Bear, M. F. (2012) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-060909-153138 · Cited by 370
Hamdan, F. F., Gauthier, J., Araki, Y., Lin, D.-T., Yoshizawa, Y., Higashi, K., Park, A.-R., Spiegelman, D., Dobrzeniecka, S., Piton, A., et al. (2011) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2011.02.001 · Cited by 349
Metadata
- Authors
- Hu, H., Qin, Y., Bochorishvili, G., Zhu, Y., van Aelst, L., & Zhu, J. J.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-07-30
- Volume
- 28
- Issue
- 31
- Pages
- 7847-7862
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2078748724
- Cited by
- 166
- References
- 16
- FWCI
- 6.86
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Hu, H., Qin, Y., Bochorishvili, G., Zhu, Y., van Aelst, L., & Zhu, J. J. (2008). Ras Signaling Mechanisms Underlying Impaired GluR1-Dependent Plasticity Associated with Fragile X Syndrome. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.1496-08.2008
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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