Sato Masaaki, Stryker Michael P
Department of Physiology, W. M. Keck Foundation Center for Integrative Neuroscience, University of California, San Francisco, San Francisco, California 94143-0444, USA.
J Neurosci. 2008 Oct 8;28(41):10278-86. doi: 10.1523/JNEUROSCI.2451-08.2008.
Sensory experience profoundly shapes neural circuitry of juvenile brain. Although the visual cortex of adult rodents retains a capacity for plasticity in response to monocular visual deprivation, the nature of this plasticity and the neural circuit changes that accompany it remain enigmatic. Here, we investigate differences between adult and juvenile ocular dominance plasticity using Fourier optical imaging of intrinsic signals in mouse visual cortex. This comparison reveals that adult plasticity takes longer than in the juvenile mouse, is of smaller magnitude, has a greater contribution from the increase in response to the open eye, and has less effect on the hemisphere ipsilateral to the deprived eye. Binocular deprivation also causes different changes in the adult. Adult plasticity is similar to juvenile plasticity in its dependence on signaling through NMDA receptors. We propose that adult ocular dominance plasticity arises from compensatory mechanisms that counterbalance the loss of afferent activity caused by visual deprivation.
感觉体验深刻地塑造了幼龄大脑的神经回路。尽管成年啮齿动物的视觉皮层在响应单眼视觉剥夺时仍具有可塑性,但这种可塑性的本质以及与之伴随的神经回路变化仍然是个谜。在这里,我们使用小鼠视觉皮层内在信号的傅里叶光学成像来研究成年和幼年眼优势可塑性之间的差异。这种比较表明,成年可塑性比幼年小鼠所需的时间更长,幅度更小,对睁眼反应增加的贡献更大,对剥夺眼同侧半球的影响更小。双眼剥夺在成年期也会引起不同的变化。成年可塑性在依赖通过NMDA受体的信号传导方面与幼年可塑性相似。我们提出,成年眼优势可塑性源于补偿机制,该机制可抵消视觉剥夺引起的传入活动丧失。