Layer 4 Gates Plasticity in Visual Cortex Independent of a Canonical Microcircuit.

Layer 4 Gates Plasticity in Visual Cortex Independent of a Canonical Microcircuit.
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DOI:
10.1016/j.cub.2020.05.067
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发表时间:
2020-08-03
期刊:
Current biology : CB
影响因子:
--
通讯作者:
McGee AW
McGee AW
中科院分区:
其他
文献类型:
--
作者:
Frantz MG;Crouse EC;Sokhadze G;Ikrar T;Stephany CÉ;Nguyen C;Xu X;McGee AW

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在发育的关键时期,中断双眼视觉会导致初级视觉皮层(V1)的眼优势(OD)发生持久变化。在这里,我们研究了这种经验依赖性可塑性是如何协调的层状电路的V1分别删除在每个皮质层(L)的基因所需的关闭关键期,nogo-66受体(ngr 1)。在L4的兴奋性神经元中删除ngr 1,而不是在L2/3,L5或L 6中,阻止了关键期的关闭,成年小鼠对短暂的单眼剥夺仍然敏感。皮质内去抑制,但不丘脑皮质去抑制伴随着这种OD可塑性。无论是幼年野生型小鼠和成年小鼠缺乏ngr 1在L4显示OD可塑性,更迅速地推进L4比L2/3或L5。有趣的是,用药物AM-251阻断L2/3的OD可塑性并不损害L5的OD可塑性。我们建议,L4限制去抑制和门OD可塑性独立的一个典型的皮质微电路。Frantz等人探索了视皮层层状回路中经验依赖性可塑性的调节和传播。第4层限制皮层内去抑制,以关闭整个视觉皮层OD可塑性的关键期。OD可塑性不遵循典型的皮质微电路。
Disrupting binocular vision during a developmental critical period can yield enduring changes to ocular dominance (OD) in primary visual cortex (V1). Here we investigated how this experience-dependent plasticity is coordinated within the laminar circuitry of V1 by deleting separately in each cortical layer (L) a gene required to close the critical period, nogo-66 receptor (ngr1). Deleting ngr1 in excitatory neurons in L4, but not in L2/3, L5, or L6, prevented closure of the critical period and adult mice remained sensitive to brief monocular deprivation. Intracortical disinhibition but not thalamocortical disinhibition accompanied this OD plasticity. Both juvenile wild-type mice and adult mice lacking ngr1 in L4 displayed OD plasticity that advanced more rapidly L4 than L2/3 or L5. Interestingly, blocking OD plasticity in L2/3 with the drug AM-251 did not impair OD plasticity in L5. We propose that L4 restricts disinhibition and gates OD plasticity independent of a canonical cortical microcircuit. Frantz et al. explore the regulation and propagation of experience-dependent plasticity within the laminar circuitry of visual cortex. Layer 4 limits intracortical disinhibition to close the critical period for OD plasticity throughout visual cortex. OD plasticity does not follow a canonical cortical microcircuit.
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