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视觉剥夺通过阻止内在可塑性的诱导来抑制 L5 锥体神经元的兴奋性。

Visual deprivation suppresses L5 pyramidal neuron excitability by preventing the induction of intrinsic plasticity.

机构信息

Department of Biology, Brandeis University, Waltham, MA 02454, USA.

出版信息

Neuron. 2010 Nov 18;68(4):750-62. doi: 10.1016/j.neuron.2010.09.033.

Abstract

In visual cortex monocular deprivation (MD) during a critical period (CP) reduces the ability of the deprived eye to activate cortex, but the underlying cellular plasticity mechanisms are incompletely understood. Here we show that MD reduces the intrinsic excitability of layer 5 (L5) pyramidal neurons and enhances long-term potentiation of intrinsic excitability (LTP-IE). Further, MD and LTP-IE induce reciprocal changes in K(v)2.1 current, and LTP-IE reverses the effects of MD on intrinsic excitability. Taken together these data suggest that MD reduces intrinsic excitability by preventing sensory-drive induced LTP-IE. The effects of MD on excitability were correlated with the classical visual system CP, and (like the functional effects of MD) could be rapidly reversed when vision was restored. These data establish LTP-IE as a candidate mechanism mediating loss of visual responsiveness within L5, and suggest that intrinsic plasticity plays an important role in experience-dependent refinement of visual cortical circuits.

摘要

在视觉皮层中,关键期(CP)的单眼剥夺(MD)会降低被剥夺眼激活皮层的能力,但潜在的细胞可塑性机制尚不完全清楚。在这里,我们表明 MD 降低了第 5 层(L5)锥体神经元的内在兴奋性,并增强了内在兴奋性的长时程增强(LTP-IE)。此外,MD 和 LTP-IE 诱导 K(v)2.1 电流的相互变化,而 LTP-IE 逆转了 MD 对内在兴奋性的影响。这些数据表明,MD 通过防止感觉驱动诱导的 LTP-IE 来降低内在兴奋性。MD 对兴奋性的影响与经典视觉系统 CP 相关,并且(与 MD 的功能影响一样)当视力恢复时,可以迅速逆转。这些数据确立了 LTP-IE 作为介导 L5 内视觉反应丧失的候选机制,并表明内在可塑性在依赖经验的视觉皮层回路细化中起着重要作用。

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