Recovery from chronic monocular deprivation following reactivation of thalamocortical plasticity by dark exposure.
Recovery from chronic monocular deprivation following reactivation of thalamocortical plasticity by dark exposure.
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DOI：
10.1038/ncomms1312
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发表时间：
2011
影响因子：
16.6
通讯作者：
Quinlan EM
中科院分区：
文献类型：
--
作者：
Montey KL;Quinlan EM
慢性单眼剥夺会导致严重弱视，这种弱视在成年后不能自发逆转。然而，成年期开始的黑暗暴露重新激活了视觉皮质中的突触可塑性，并促进了慢性单眼剥夺的恢复。在这里，我们发现慢性单眼剥夺显着降低了前馈兴奋的强度，并显着降低了剥夺双眼视觉皮质中树突棘的密度。黑暗暴露后的反向剥夺显著增强了丘脑皮质突触传递的强度，并显著增加了视皮层深处主神经元上树突棘的密度。因此，在慢性单眼剥夺的恢复过程中，黑暗暴露重新激活了成人视觉皮质中广泛存在的突触可塑性，包括丘脑皮质突触。
Chronic monocular deprivation induces severe amblyopia that is resistant to spontaneous reversal in adulthood. However, dark exposure initiated in adulthood reactivates synaptic plasticity in the visual cortex and promotes recovery from chronic monocular deprivation. Here we show that chronic monocular deprivation significantly decreases the strength of feedforward excitation and significantly decreases the density of dendritic spines throughout the deprived binocular visual cortex. Dark exposure followed by reverse deprivation significantly enhances the strength of thalamocortical synaptic transmission and the density of dendritic spines on principle neurons throughout the depth of the visual cortex. Thus dark exposure reactivates widespread synaptic plasticity in the adult visual cortex, including at thalamocortical synapses, during the recovery from chronic monocular deprivation.