Failed stabilization for long-term potentiation in the auditory cortex of FMR1 knockout mice

Fragile X syndrome is a developmental disorder that affects sensory systems. A null mutation of the Fragile X Mental Retardation protein 1 (Fmr1) gene in mice has varied effects on developmental plasticity in different sensory systems, including normal barrel cortical plasticity, altered ocular domi...

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Published inPloS one Vol. 9; no. 8; p. e104691
Main Authors Yang, Sungchil, Yang, Sunggu, Park, Jae-Sung, Kirkwood, Alfredo, Bao, Shaowen
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 12.08.2014
Public Library of Science (PLoS)
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Summary:Fragile X syndrome is a developmental disorder that affects sensory systems. A null mutation of the Fragile X Mental Retardation protein 1 (Fmr1) gene in mice has varied effects on developmental plasticity in different sensory systems, including normal barrel cortical plasticity, altered ocular dominance plasticity and grossly impaired auditory frequency map plasticity. The mutation also has different effects on long-term synaptic plasticity in somatosensory and visual cortical neurons, providing insights on how it may differentially affect the sensory systems. Here we present evidence that long-term potentiation (LTP) is impaired in the developing auditory cortex of the Fmr1 knockout (KO) mice. This impairment of synaptic plasticity is consistent with impaired frequency map plasticity in the Fmr1 KO mouse. Together, these results suggest a potential role of LTP in sensory map plasticity during early sensory development.
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Conceived and designed the experiments: Sungchil Yang Sunggu Yang AK SB. Performed the experiments: Sungchil Yang Sunggu Yang JP. Analyzed the data: Sungchil Yang Sunggu Yang. Contributed reagents/materials/analysis tools: JP AK. Contributed to the writing of the manuscript: Sungchil Yang Sunggu Yang AK SB.
Competing Interests: The authors have declared that no competing interests exist.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0104691