Input-specific critical periods for experience-dependent plasticity in layer 2/3 pyramidal neurons.

Input-specific critical periods for experience-dependent plasticity in layer 2/3 pyramidal neurons.
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DOI:
10.1523/jneurosci.6042-10.2011
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发表时间:
2011-03-23
期刊:
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子:
--
通讯作者:
Barth AL
Barth AL
中科院分区:
其他
文献类型:
--
作者:
Wen JA;Barth AL

文献摘要

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经验依赖可塑性的关键时期已经在感觉皮层中得到了很好的表征,在那里,改变的感觉输入驱动放电率变化的能力已经在整个大脑区域得到了证明。本研究表明,小鼠初级体感皮层兴奋性突触强度的快速经验依赖性变化在第2/3层锥体神经元中表现出输入特异性和机制差异的关键时期。去除除单个须外的所有须(单须体验;SWE)可以在出生后第二和第三周的一个短窗口内触发个体谷氨酸能突触接触到2/3层神经元的加强。在第4层和假定的2/3输入中,sw触发的可塑性具有离散的开始,在此之前它不能被诱导。出生后第三周开始后,两种输入都结束了sw突触的强化,这表明两种输入都出现了经验依赖可塑性的关键期。重要的是,对于2/3-2/3层和4-2/3层兴奋性突触来说,这个关键时期的时间既延迟又延长。此外,第2/3层输入的可塑性不会引起钙渗透的、缺乏glur2的ampar的运输,而第4层输入有时会这样做。尽管第4层和第2/3层突触沿着树突紧密相连,但关键时期时间和可塑性机制的分离表明,体内可塑性的发育调节具有显著的特异性。
Critical periods for experience-dependent plasticity have been well-characterized within sensory cortex, where the ability of altered sensory input to drive firing rate changes has been demonstrated across brain areas. Here we show that rapid experience-dependent changes in the strength of excitatory synapses within mouse primary somatosensory cortex exhibit a critical period that is input-specific and mechanistically distinct in layer 2/3 pyramidal neurons. Removal of all but a single whisker (single whisker experience; SWE) can trigger the strengthening of individual glutamatergic synaptic contacts onto layer 2/3 neurons only during a short window during the second and third postnatal week. At both layer 4 and putative 2/3 inputs, SWE-triggered plasticity has a discrete onset, before which it cannot be induced. SWE-synaptic strengthening is concluded at both inputs after the beginning of the third postnatal week, indicating that both types of inputs display a critical period for experience-dependent plasticity. Importantly, the timing of this critical period is both delayed and prolonged for layer 2/3-2/3 versus layer 4-2/3 excitatory synapses. Furthermore, plasticity at layer 2/3 inputs does not invoke the trafficking of calcium-permeable, GluR2-lacking AMPARs, whereas it sometimes does at layer 4 inputs. The dissociation of critical period timing and plasticity mechanisms at layer 4 and layer 2/3 synapses, despite the close apposition of these inputs along the dendrite, suggests remarkable specificity for the developmental regulation of plasticity in vivo.