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在成年小鼠中跨模态恢复眼优势可塑性。

Cross-modal restoration of ocular dominance plasticity in adult mice.

机构信息

Institute of General Zoology and Animal Physiology, Jena, Germany.

出版信息

Eur J Neurosci. 2018 Jun;47(11):1375-1384. doi: 10.1111/ejn.13944. Epub 2018 Jun 1.

Abstract

The temporal closure of one eye in juvenile and young adult mice induces a shift of the ocular dominance (OD) of neurons in the binocular visual cortex. However, OD plasticity typically declines with age and is completely absent in matured mice beyond postnatal day (PD) 110. As it has been shown that the deprivation of one sensory input can induce neuronal alterations in non-deprived sensory cortices, we here investigated whether cross-modal interactions have the potential to reinstall OD plasticity in matured mice. Strikingly, using intrinsic signal imaging we could demonstrate that both whisker deprivation and auditory deprivation for only one week reinstated OD plasticity in fully adult mice. These OD shifts were always mediated by an increase of V1 responsiveness to visual stimulation of the open eye, a characteristic feature of OD plasticity normally only found in young adult mice. Moreover, systemic administration of the competitive NMDA receptor antagonist CPP completely abolished cross-modally induced OD plasticity. Taken together, we demonstrate here for the first time that the deprivation of non-visual senses has the potential to rejuvenate the adult visual cortex.

摘要

幼年和年轻成年小鼠一只眼的暂时封闭会引起双眼视觉皮层中神经元的眼优势(OD)转移。然而,OD 可塑性通常随着年龄的增长而下降,在出生后第 110 天(PD)之后的成熟小鼠中完全不存在。由于已经表明剥夺一种感觉输入可以在未剥夺感觉皮层中诱导神经元改变,因此我们在这里研究了跨模态相互作用是否有可能在成熟小鼠中重新安装 OD 可塑性。令人惊讶的是,使用内源信号成像,我们可以证明仅一周的胡须剥夺和听觉剥夺即可使完全成年的小鼠重新建立 OD 可塑性。这些 OD 转变总是通过增加 V1 对睁开眼睛的视觉刺激的反应来介导的,这是 OD 可塑性的一个特征,通常仅在年轻成年小鼠中发现。此外,系统给予竞争性 NMDA 受体拮抗剂 CPP 可完全消除跨模态诱导的 OD 可塑性。总之,我们在这里首次证明,非视觉感觉的剥夺有可能使成年视觉皮层恢复活力。

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