Molecular mechanism for loss of visual cortical responsiveness following brief monocular deprivation
Molecular mechanism for loss of visual cortical responsiveness following brief monocular deprivation
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DOI：
10.1038/nn1100
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发表时间：
2003-08-01
影响因子：
25
通讯作者：
Bear, MF
中科院分区：
文献类型：
--
作者：
Heynen, AJ;Yoon, BJ;Bear, MF
在出生后早期，当一只眼睛暂时丧失视觉时，视觉皮层中出现了一种戏剧性的经验依赖性突触可塑性。单眼剥夺（MD）改变了突触传递，使得皮层神经元停止对剥夺眼睛的刺激作出反应，但这是如何发生的知之甚少。在这里，我们表明，在大鼠视觉皮层，简短的MD集运动相同的分子和功能的变化，同突触长期抑郁症（LTD）的实验模型，和先前的突触抑郁症由MD闭塞随后的诱导有限公司。LTD的机制，现在有一个详细的了解，因此有助于视觉皮层可塑性。
A dramatic form of experience-dependent synaptic plasticity is revealed in visual cortex when one eye is temporarily deprived of vision during early postnatal life. Monocular deprivation (MD) alters synaptic transmission such that cortical neurons cease to respond to stimulation of the deprived eye, but how this occurs is poorly understood. Here we show in rat visual cortex that brief MD sets in motion the same molecular and functional changes as the experimental model of homosynaptic long-term depression (LTD), and that prior synaptic depression by MD occludes subsequent induction of LTD. The mechanisms of LTD, about which there is now a detailed understanding, therefore contribute to visual cortical plasticity.