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Spatial mapping of activity changes across sensory areas following visual deprivation in adults.
Journal of Neuroscience ( IF 4.4 ) Pub Date : 2024-11-26 , DOI: 10.1523/jneurosci.0969-24.2024 Samuel Parkins,Yidong Song,Yanis Jaoui,Aryan Gala,Kaven T Konda,Crispo Richardson,Hey-Kyoung Lee
Journal of Neuroscience ( IF 4.4 ) Pub Date : 2024-11-26 , DOI: 10.1523/jneurosci.0969-24.2024 Samuel Parkins,Yidong Song,Yanis Jaoui,Aryan Gala,Kaven T Konda,Crispo Richardson,Hey-Kyoung Lee
Loss of a sensory modality triggers global adaptation across brain areas, allowing the remaining senses to guide behavior more effectively. There are specific synaptic and circuit plasticity observed across many sensory areas, which suggests potential widespread changes in activity. Here we used a cFosTRAP2 mouse line to drive tdTomato (tdT) expression in active cells to spatially map the extent of activity changes in various sensory areas in adult mice of both sexes following two modes of visual deprivation. We found that in the primary visual cortex (V1) both dark exposure (DE) and enucleation (EN) caused an initial loss of active cells followed by a partial rebound, which occurred relatively more in the superficial layers. A similar pattern was observed in the secondary visual cortex, especially in the lateral areas (V2L). The spared primary sensory cortices adapted distinctly. In the primary somatosensory barrel cortex (S1BF) there was a change in the density of active cells dependent on the duration and the mode of visual deprivation. In the primary auditory cortex (A1), there was a relative reduction in the density of active cells in the superficial layers without a significant change in the overall density. There were minimal changes in the active cell density in the secondary cortices of the spared senses and the multisensory retrosplenial cortex (RSP). Our results are consistent with cross-modal recruitment of the deprived visual cortex and compensatory plasticity in the spared primary sensory cortices that can support enhanced processing and refinement of the spared senses.Significance Statement The neural basis for improved processing of the spared senses after losing vision is largely dependent on plasticity mechanisms driven by neural activity. Using a transgenic mouse model to label active neurons in a temporally controlled manner, this study reveals the spatial pattern of widespread activity changes across brain areas following visual deprivation in adult mice. The findings suggest that the deprived visual cortex undergoes an initial reduction in activity followed by a rebound suggestive of cross-modal recruitment. Activity changes in the spared primary sensory cortices conform to compensatory plasticity, which could support improved processing of the spared senses. The results highlight the presence of large-scale plasticity in the adult brain to compensate for loss of vision.
中文翻译:
成人视觉剥夺后感觉区域活动变化的空间映射。
感觉模式的丧失会触发跨大脑区域的整体适应,使剩余的感官能够更有效地指导行为。在许多感觉区域观察到特定的突触和回路可塑性,这表明活动可能发生广泛的变化。在这里,我们使用 cFosTRAP2 小鼠系来驱动活性细胞中的 tdTomato (tdT) 表达,以在空间上绘制两种视觉剥夺模式后两性成年小鼠各个感觉区域的活动变化程度。我们发现,在初级视觉皮层 (V1) 中,暗暴露 (DE) 和剜除 (EN) 都会导致活性细胞的初始丢失,然后是部分反弹,这在表层发生得相对较多。在次级视觉皮层中观察到类似的模式,尤其是在外侧区域 (V2L)。幸免的初级感觉皮层明显适应。在初级体感桶皮层 (S1BF) 中,活性细胞的密度发生了变化,具体取决于视觉剥夺的持续时间和模式。在初级听觉皮层 (A1) 中,浅表层活动细胞的密度相对降低,整体密度没有显着变化。备用感觉的次级皮层和多感觉脾后皮层 (RSP) 的活性细胞密度变化很小。我们的结果与被剥夺的视觉皮层的跨模态募集和未受保留的初级感觉皮层中的代偿可塑性一致,这可以支持未受剥夺感觉的增强处理和细化。意义陈述 丧失视力后改善剩余感官处理的神经基础在很大程度上取决于神经活动驱动的可塑性机制。 本研究使用转基因小鼠模型以时间控制的方式标记活跃的神经元,揭示了成年小鼠视力剥夺后大脑区域广泛活动变化的空间模式。研究结果表明,被剥夺的视觉皮层最初活动减少,然后反弹,提示跨模态募集。备用初级感觉皮层的活动变化符合代偿可塑性,这可以支持改善备用感觉的处理。结果突出了成人大脑中存在大规模的可塑性,以补偿视力的丧失。
更新日期:2024-11-26
中文翻译:
成人视觉剥夺后感觉区域活动变化的空间映射。
感觉模式的丧失会触发跨大脑区域的整体适应,使剩余的感官能够更有效地指导行为。在许多感觉区域观察到特定的突触和回路可塑性,这表明活动可能发生广泛的变化。在这里,我们使用 cFosTRAP2 小鼠系来驱动活性细胞中的 tdTomato (tdT) 表达,以在空间上绘制两种视觉剥夺模式后两性成年小鼠各个感觉区域的活动变化程度。我们发现,在初级视觉皮层 (V1) 中,暗暴露 (DE) 和剜除 (EN) 都会导致活性细胞的初始丢失,然后是部分反弹,这在表层发生得相对较多。在次级视觉皮层中观察到类似的模式,尤其是在外侧区域 (V2L)。幸免的初级感觉皮层明显适应。在初级体感桶皮层 (S1BF) 中,活性细胞的密度发生了变化,具体取决于视觉剥夺的持续时间和模式。在初级听觉皮层 (A1) 中,浅表层活动细胞的密度相对降低,整体密度没有显着变化。备用感觉的次级皮层和多感觉脾后皮层 (RSP) 的活性细胞密度变化很小。我们的结果与被剥夺的视觉皮层的跨模态募集和未受保留的初级感觉皮层中的代偿可塑性一致,这可以支持未受剥夺感觉的增强处理和细化。意义陈述 丧失视力后改善剩余感官处理的神经基础在很大程度上取决于神经活动驱动的可塑性机制。 本研究使用转基因小鼠模型以时间控制的方式标记活跃的神经元,揭示了成年小鼠视力剥夺后大脑区域广泛活动变化的空间模式。研究结果表明,被剥夺的视觉皮层最初活动减少,然后反弹,提示跨模态募集。备用初级感觉皮层的活动变化符合代偿可塑性,这可以支持改善备用感觉的处理。结果突出了成人大脑中存在大规模的可塑性,以补偿视力的丧失。