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首页> 外文期刊>Journal of Neurophysiology >Early postnatal plasticity in neocortex of Fmr1 knockout mice.
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Early postnatal plasticity in neocortex of Fmr1 knockout mice.

机译：Fmr1基因敲除小鼠新皮层的早期产后可塑性。

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摘要

Fragile X syndrome is produced by a defect in a single X-linked gene, called Fmr1, and is characterized by abnormal dendritic spine morphologies with spines that are longer and thinner in neocortex than those from age-matched controls. Studies using Fmr1 knockout mice indicate that spine abnormalities are especially pronounced in the first month of life, suggesting that altered developmental plasticity underlies some of the behavioral phenotypes associated with the syndrome. To address this issue, we used intracellular recordings in neocortical slices from early postnatal mice to examine the effects of Fmr1 disruption on two forms of plasticity active during development. One of these, long-term potentiation of intrinsic excitability, is intrinsic in expression and requires mGluR5 activation. The other, spike timing-dependent plasticity, is synaptic in expression and requires N-methyl-d-aspartate receptor activation. While intrinsic plasticity was normal in the knockout mice, synaptic plasticity was altered in an unusual and striking way: long-term depression was robust but long-term potentiation was entirely absent. These findings underscore the ideas that Fmr1 has highly selective effects on plasticity and that abnormal postnatal development is an important component of the disorder.
机译：脆弱的X综合征是由单个X连锁基因Fmr1的缺陷产生的，其特征是树突棘形态异常，新皮层中的棘比年龄匹配的对照组更长，更细。使用Fmr1基因敲除小鼠的研究表明，脊柱异常在生命的第一个月尤为明显，这表明发育可塑性的改变是与该综合征相关的某些行为表型的基础。为了解决这个问题，我们使用了来自出生后早期小鼠的新皮质切片中的细胞内记录来检查Fmr1破坏对发育过程中活跃的两种形式的可塑性的影响。这些是内在兴奋性的长期增强之一，在表达中是内在的，需要mGluR5激活。另一类是尖峰时间依赖的可塑性，在表达上是突触的，需要激活N-甲基-d-天冬氨酸受体。虽然敲除小鼠的内在可塑性是正常的，但突触可塑性却以一种不寻常且惊人的方式改变：长期压抑是有力的，但长期缺乏增强作用。这些发现强调了Fmr1对可塑性具有高度选择性的作用，而异常的产后发育是该疾病的重要组成部分。

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