Sensory experience during locomotion promotes recovery of function in adult visual cortex.
Sensory experience during locomotion promotes recovery of function in adult visual cortex.
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DOI：
10.7554/elife.02798
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发表时间：
2014-06-26
期刊：
影响因子：
7.7
通讯作者：
Stryker MP
中科院分区：
文献类型：
--
作者：
Kaneko M;Stryker MP
在成年人的视觉皮层中，感觉剥夺的恢复是缓慢和不完全的。在这项研究中，我们表明，视觉刺激在运动过程中，这增加了初级视觉皮层的视觉反应的增益，大大提高了小鼠的恢复。兴奋性神经元恢复了正常的反应水平，而窄峰（抑制性）神经元仍然不太活跃。视觉刺激或运动本身并不能促进恢复。动物在运动过程中看到的特定视觉刺激的反应得到恢复，而对另一种正常有效刺激的反应则没有，这表明运动只促进与运动同时激活的神经回路的恢复。这些发现可能为改善人类弱视的恢复提供了一条途径。http://dx.doi.org/10.7554/eLife.02798.001弱视，也被称为“懒惰的眼睛”，是一种在儿童时期视力无法正常发展的情况，不是由于眼睛本身的问题，而是由于从眼睛到大脑的信息传输出现问题。当诸如斜视（两眼指向不同的方向）之类的疾病导致大脑持续忽略一只眼睛的输入时，就会发生这种情况，结果是这只眼睛的视力永远不会完全发育。如果在婴儿期发现，弱视可以通过手术治疗，尽管这种干预措施必须尽早进行，因为它们在成人身上的效果要差得多。然而，Kaneko和斯特赖克现在提出的数据表明，成年哺乳动物的视觉系统可能比以前认为的更容易改变。在幼鼠视觉系统发育的关键时期，通过缝合眼睑，剥夺了幼鼠一只眼睛的视觉输入。当眼睛在4-5个月大时重新睁开时，小鼠在对应于该眼睛的大脑区域中显示出减少的反应。然而，如果让这些老鼠每天在跑步机上跑几个小时，同时观察视觉刺激，无论是黑色和白色光栅还是随机噪音，它们被剥夺的眼睛的视力都会显示出快速和惊人的改善。这种改善在没有视觉刺激的小鼠中没有观察到，或者在观察视觉刺激但不跑步的小鼠中没有观察到。此外，这种改善是针对跑步时看到的特定刺激的。尽管这种效应背后的机制尚不清楚，但人们知道跑步会增加神经元的活动，一种可能性是那些异常活跃的神经元（如编码视觉刺激的神经元）彼此之间形成了更强的联系：“一起激发的神经元连接在一起”。还需要进一步的研究来确定人类视觉系统是否会发生类似的变化，如果是的话，它们是否可以应用于弱视的治疗。DOI：http://dx.doi.org/10.7554/eLife.02798.002网站
Recovery from sensory deprivation is slow and incomplete in adult visual cortex. In this study, we show that visual stimulation during locomotion, which increases the gain of visual responses in primary visual cortex, dramatically enhances recovery in the mouse. Excitatory neurons regained normal levels of response, while narrow-spiking (inhibitory) neurons remained less active. Visual stimulation or locomotion alone did not enhance recovery. Responses to the particular visual stimuli viewed by the animal during locomotion recovered, while those to another normally effective stimulus did not, suggesting that locomotion promotes the recovery only of the neural circuits that are activated concurrent with the locomotion. These findings may provide an avenue for improving recovery from amblyopia in humans. DOI: http://dx.doi.org/10.7554/eLife.02798.001 Amblyopia, otherwise known as ‘lazy eye’, is a condition in which vision fails to develop normally during childhood, not due to problems with the eye itself but due to problems with the transmission of information from the eye to the brain. It occurs when disorders such as squint—in which the eyes point in different directions—cause the brain to continually ignore input from one eye, with the result that vision in that eye never fully develops. If detected in infancy, amblyopia can be treated by surgery, although such interventions must be performed early because they are much less effective when used on adults. However, Kaneko and Stryker now present data suggesting that the adult mammalian visual system may be more amenable to change than previously thought. Young mice were deprived of visual input to one eye, by having an eyelid sewn shut, during a critical period in the development of their visual systems. When the eye was re-opened at the age of 4–5 months, the mice showed reduced responses in the brain region corresponding to that eye. However, if the mice were then allowed to run on a treadmill for several hours a day while viewing a visual stimulus—either black and white gratings or random noise—the vision in their deprived eye showed a rapid and striking improvement. This improvement was not seen in mice that ran without a visual stimulus, or in mice that looked at the visual stimulus but did not run. Moreover, the improvement was specific to the particular stimulus viewed whilst running. Although the mechanism behind this effect is unclear, it is known that running increases neuronal activity, and one possibility is that neurons that are active simultaneously—such as those encoding the visual stimulus—form stronger connections with one another: ‘neurons that fire together, wire together’. Further work is required to determine whether similar changes occur in the human visual system and, if they do, whether they could be applied to the treatment of amblyopia. DOI: http://dx.doi.org/10.7554/eLife.02798.002