成年期发病的听觉剥夺增强视觉皮层神经反应的衰减并改善周边视力

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中文摘要

在整个生命周期中，大脑发生可塑性变化的能力对于优化其与环境的相互作用至关重要。对感觉丧失的适应表现为：被保留的感觉跨模态征用失去自身感觉输入的皮层区域，以及被保留皮层区域的代偿性可塑性。前者被认为增加了处理与被保留模态相关信息所需的皮层资源，后者被认为可精细化被保留的感觉。在动物模型中，已在被剥夺的初级感觉皮层和被保留的初级感觉皮层中观察到突触和环路水平的可塑性。在本研究中，我们考察了在雌雄成年小鼠中启动的跨模态听觉剥夺如何使初级视觉皮层（V1）发生适应。为此，我们使用双光子钙成像记录V1第2/3层（L2/3）的刺激诱发神经活动，并呈现仅局限于中央或周边视野的视觉刺激。我们发现，成年期发病的耳聋增强了对一系列刺激的刺激诱发反应的衰减，主要发生在代表周边单眼视野的内侧V1，而未影响群体解码能力。此外，成年期发病的耳聋小鼠在检测静态光栅的周边视力方面表现出选择性行为改善，而检测移动光栅的对比敏感度没有变化。我们的发现提示，神经衰减的增强可能支持成年V1的代偿性可塑性，这可能有利于刺激编码效率，从而改善对精细周边视觉特征的检测。意义声明：丧失一种感觉模态会导致广泛的大脑适应以增强剩余的感觉。除了跨模态征用（将被剥夺的大脑区域重新用于处理被保留的感觉）之外，被保留感觉区域还存在功能性精细化，称为代偿性可塑性。虽然可塑性在早发性感觉丧失中较为显著，但在成年期发病的感觉丧失后也观察到功能代偿。在此，我们报告，小鼠成年期发病的耳聋加重了视觉皮层对视觉刺激反应的衰减，尤其是在周边视野，并有编码更高效的迹象。此外，耳聋的成年小鼠在周边视力方面表现出相当选择性的改善。我们的研究提示了成年视觉皮层代偿性可塑性的一种机制，这可能有利于视觉功能。

英文摘要

The ability of the brain to undergo plastic changes throughout the lifespan of an organism is essential to optimize its interactions with its environment. Adaptation to sensory loss is observed as cross-modal recruitment of the cortical areas deprived of their own sensory inputs by the spared senses and as compensatory plasticity of the spared cortical areas. The former is thought to increase the cortical resource for processing information related to the spared modalities and the latter is thought to refine the spared senses. In animal models, synaptic and circuit-level plasticity have been observed in both the deprived primary sensory cortex and in the spared primary sensory cortices. In this study, we examined how the primary visual cortex (V1) adapts to cross-modal auditory deprivation initiated in adult mice of both sexes. To do this, we recorded the stimulus-evoked neural activity in V1 layer 2/3 (L2/3) using 2-photon calcium imaging and presented visual stimuli restricted to either the central or the peripheral visual field. We found that adult-onset deafening intensified the attenuation of stimulus-evoked responses to a range of stimuli, largely in the medial V1 representing the peripheral monocular visual field, without affecting the population decoding capability. Furthermore, adult-onset deaf mice exhibited selective behavioral improvement on peripheral visual acuity for detecting static gratings, without changes in contrast sensitivity for detecting moving gratings. Our findings suggest enhancement of neural attenuation may support compensatory plasticity in adult V1, which may benefit the stimulus encoding efficiency to improve detection of fine peripheral visual features.Significance Statement Losing a sensory modality leads to widespread brain adaptation to enhance the remaining senses. In addition to cross-modal recruitment, which repurposes the deprived brain areas to process the spared senses, there is functional refinement of the spared sensory areas referred to as compensatory plasticity. While plasticity is prominent for early-onset sensory loss, functional compensation is also observed after adult-onset sensory loss. Here, we report that adult-onset deafness in mice accentuates attenuation of visual cortical responses to visual stimuli, especially in the peripheral visual field, with indications of more efficient coding. Additionally, deafened adult mice show rather selective improvement on peripheral visual acuity. Our study suggests a mechanism of compensatory plasticity in the adult visual cortex, which may benefit visual function.