Plasticity of cortical neurons in the developing visual cortex.

哺乳动物新大脑皮层的神经回路在出生后发育过程中被经验诱导的神经活动所改变。出生后早期的单眼剥夺改变了初级视皮层的神经回路，使得大多数神经元对给予被剥夺眼的刺激反应不佳，来自这只眼的丘脑输入最终被收回。尽管这种重建被认为是在皮质IV层的丘脑皮质突触开始的，但最近的实验表明，生理可塑性在颗粒上层比皮质IV层更早进行。这些发现表明，丘脑皮质的重组可能是由皮质内连接的早期变化所引导的。然而，皮质回路中的哪种类型的修饰是颗粒上层快速可塑性的基础仍是未知的。为了解决这个问题，本研究旨在探索皮质内从第IV层到第III层的上升轴突的形态可塑性，它为颗粒上细胞提供强大的兴奋性输入。我们还检测了在神经突起延伸中起作用的神经营养因子的皮质含量。内在信号的光学成像使我们能够识别眼优势柱，并在眼优势柱的边缘注入逆行示踪剂III。通过在MD前后的同一位置注射两种逆行示踪剂，我们检查了标记的第四层细胞的分布与眼优势柱模式相关的可能的变化。MD后部分病例剥夺眼柱内标记细胞减少。MD还降低了视觉皮质中脑源性神经营养因子的蛋白水平。这些结果表明，MD可能导致服务于剥夺眼的皮质内轴突的收缩，而BDNF可能参与了这种收缩。

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.