Failed Stabilization for Long-Term Potentiation in the Auditory Cortex of Fmr1 Knockout Mice

نویسندگان

  • Sungchil Yang
  • Sunggu Yang
  • Jae-Sung Park
  • Alfredo Kirkwood
  • Shaowen Bao
چکیده

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.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Increased Threshold for Spike-Timing-Dependent Plasticity Is Caused by Unreliable Calcium Signaling in Mice Lacking Fragile X Gene Fmr1

Fragile X syndrome, caused by a mutation in the Fmr1 gene, is characterized by mental retardation. Several studies reported the absence of long-term potentiation (LTP) at neocortical synapses in Fmr1 knockout (FMR1-KO) mice, but underlying cellular mechanisms are unknown. We find that in the prefrontal cortex (PFC) of FMR1-KO mice, spike-timing-dependent LTP (tLTP) is not so much absent, but ra...

متن کامل

Altered hippocampal synaptic plasticity in the FMR1 gene family knockout mouse models.

Fragile X syndrome (FXS) is the most common form of inherited mental retardation. The syndrome results from the absence of the fragile X mental retardation protein (FMRP), which is encoded by the fragile X mental retardation 1 (FMR1) gene. FMR1 and its two paralogs, fragile X-related genes 1 and 2 (FXR1 and -2), form the Fmr1 gene family. Here, we examined long-lasting synaptic plasticity in Fm...

متن کامل

Action of brain-derived neurotrophic factor on function and morphology of visual cortical neurons

Brain-derived neurotrophic factor (BDNF) is known to play a role in experience-dependent plasticity of the developing visual cortex. For example, BDNF acutely enhances long-term potentiation and blocks long-term depression in the visual cortex of young rats. Such acute actions of BDNF suggested to be mediated mainly through presynaptic mechanisms. A chronic application of BDNF to the visual cor...

متن کامل

Action of brain-derived neurotrophic factor on function and morphology of visual cortical neurons

Brain-derived neurotrophic factor (BDNF) is known to play a role in experience-dependent plasticity of the developing visual cortex. For example, BDNF acutely enhances long-term potentiation and blocks long-term depression in the visual cortex of young rats. Such acute actions of BDNF suggested to be mediated mainly through presynaptic mechanisms. A chronic application of BDNF to the visual cor...

متن کامل

Reversal of activity-mediated spine dynamics and learning impairment in a mouse model of Fragile X syndrome.

Fragile X syndrome (FXS) is characterized by intellectual disability and autistic traits, and results from the silencing of the FMR1 gene coding for a protein implicated in the regulation of protein synthesis at synapses. The lack of functional Fragile X mental retardation protein has been proposed to result in an excessive signaling of synaptic metabotropic glutamate receptors, leading to alte...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 9  شماره 

صفحات  -

تاریخ انتشار 2014