Plasticity of cortical neurons in the developing visual cortex.

哺乳动物新皮质中的神经回路在出生后发育过程中通过经验诱发的神经活动而改变。出生后早期的单眼剥夺（MD）会重塑初级视觉皮层的神经回路，因此大多数神经元对被剥夺的眼睛的刺激反应不佳，并且来自该眼睛的丘脑输入最终会缩回。尽管这种重塑被认为是在皮质第四层的丘脑皮质突触处启动的，但最近的实验表明，生理可塑性在皮质的颗粒上层比在皮质的第四层中进行得更早。这些发现表明丘脑皮质重组可能是由皮质内连接的早期变化引导的。然而，目前尚不清楚皮质回路的何种类型的修饰是颗粒上层快速可塑性的基础。为了解决这个问题，本研究旨在探索第四层至第三层皮质内上升轴突的形态可塑性，这些轴突为颗粒上细胞提供强烈的兴奋性输入。我们还检查了在神经突延伸中发挥作用的神经营养素的皮质含量。内在信号的光学成像使我们能够识别眼优势柱，并在眼优势柱的边界注入逆行示踪剂内层 III。通过在 MD 之前和之后在同一位置注射两种逆行示踪剂，我们检查了标记的 IV 层细胞分布相对于眼优势柱模式的可能变化。在某些情况下，MD 后被剥夺的眼列中标记的细胞数量减少。 MD 还降低了视觉皮层中脑源性神经营养因子的蛋白质水平。这些结果表明，MD 可能会导致服务于被剥夺眼睛的皮质内轴突回缩，而 BDNF 可能会导致该回缩。

Neural circuits in the mammalian neocortex are modified by experience-induced neural activity during postnatal development. Monocular deprivation (MD) during early postnatal life remodels neural circuits of the primary visual cortex so that most neurons respond poorly to stimuli presented to the deprived eye and thalamic input from this eye is ultimately retracted. Although this remodeling has been thought to be initiated at thalamocortical synapses in cortical layer IV, recent experiments showed that physiological plasticity proceeds earlier in supragranular layers than in layer IV of the cortex. These findings suggest a possibility that thalamocortical reorganization is guided by earlier changes in intracortical connections. However, it is still unknown what type of modification in the cortical circuit underlies this rapid plasticity in supragranular layers. To address this question, the present research aimed to explore morphological plasticity of the intracortical ascending axons from layer IV to III, which give strong excitatory inputs to supragranular cells. Also we examined cortical content of neurotrophins which play a role in neurite extension. Optical imaging of the intrinsic signal allowed us to identify the ocular dominance columns and to inject a retrograde tracer inlayer III at the border of the ocular dominance columns. By injecting two retrograde tracers at the same location before and after MD, we examined a possible change in the distribution of labeled layer IV cells in relation to the ocular dominance column pattern. The number of labeled cells decreased in the deprived eye columns after MD in some cases. MD also decreased protein level of brain-derived neurotrophic factor in the visual cortex. These results show a possibility that MD might induce a retraction of intracortical axons serving the deprived eye and that BDNF might contribute to the retraction.