Abstract
Evidence is reviewed that the consequences of group 1 metabotropic glutamate receptor (Gp1 mGluR) activation are exaggerated in the absence of the fragile X mental retardation protein, likely reflecting altered dendritic protein synthesis. Abnormal mGluR signaling could be responsible for remarkably diverse psychiatric and neurological symptoms in fragile X syndrome, including delayed cognitive development, seizures, anxiety, movement disorders and obesity.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Anxiety Disorders / genetics
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Anxiety Disorders / metabolism
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Anxiety Disorders / physiopathology
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Brain / metabolism*
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Brain / physiopathology
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Child
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Developmental Disabilities / genetics
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Developmental Disabilities / metabolism
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Developmental Disabilities / physiopathology
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Epilepsy / genetics
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Epilepsy / metabolism
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Epilepsy / physiopathology
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Fragile X Mental Retardation Protein
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Fragile X Syndrome / metabolism*
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Fragile X Syndrome / physiopathology
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Fragile X Syndrome / therapy
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Humans
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Movement Disorders / genetics
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Movement Disorders / metabolism
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Movement Disorders / physiopathology
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Nerve Tissue Proteins / genetics
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Nerve Tissue Proteins / metabolism*
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RNA-Binding Proteins / genetics
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RNA-Binding Proteins / metabolism*
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Receptors, Metabotropic Glutamate / biosynthesis*
Substances
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FMR1 protein, human
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Nerve Tissue Proteins
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RNA-Binding Proteins
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Receptors, Metabotropic Glutamate
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Fragile X Mental Retardation Protein