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在眼优势可塑性过程中,胼胝体输入对剥夺眼反应的功能掩蔽。

Functional masking of deprived eye responses by callosal input during ocular dominance plasticity.

机构信息

Istituto di Neuroscienze, Consiglio Nazionale delle Ricerche, via G. Moruzzi 1, 56100 Pisa, Italy.

出版信息

Neuron. 2009 Dec 10;64(5):707-18. doi: 10.1016/j.neuron.2009.10.019.

DOI:10.1016/j.neuron.2009.10.019
PMID:20005826
Abstract

Monocular deprivation (MD) is a well-known paradigm of experience-dependent plasticity in which cortical neurons exhibit a shift of ocular dominance (OD) toward the open eye. The mechanisms underlying this form of plasticity are incompletely understood. Here we demonstrate the involvement of callosal connections in the synaptic modifications occurring during MD. Rats at the peak of the critical period were deprived for 7 days, resulting in the expected OD shift toward the open eye. Acute microinjection of the activity blocker muscimol into the visual cortex contralateral to the recording site restored binocularity of cortical cells. Continuous silencing of callosal input throughout the period of MD also resulted in substantial attenuation of the OD shift. Blockade of interhemispheric communication selectively enhanced deprived eye responses with no effect on open eye-driven activity. We conclude that callosal inputs play a key role in functional weakening of less active connections during OD plasticity.

摘要

单眼剥夺(MD)是一种众所周知的经验依赖性可塑性范例,其中皮质神经元表现出对开放眼的眼优势(OD)的转变。这种形式的可塑性的机制尚不完全清楚。在这里,我们证明了胼胝体连接在 MD 期间发生的突触修饰中的作用。在关键期高峰期的大鼠被剥夺 7 天,导致预期的 OD 向开眼的转变。在记录部位对侧的视皮层中急性微注射活性阻断剂毒蕈碱可恢复皮质细胞的双眼性。在 MD 期间持续沉默胼胝体输入也导致 OD 转变的大幅度衰减。半球间通讯的阻断选择性地增强了剥夺眼的反应,而对开眼驱动的活动没有影响。我们得出结论,胼胝体输入在 OD 可塑性期间对不活跃连接的功能减弱起着关键作用。

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