Plasticity of cortical neurons in the developing visual cortex.

哺乳动物新皮层中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修饰。出生后早期的单眼剥夺（MD）重塑了初级视觉皮层的神经回路，使得大多数神经元对被剥夺的眼睛的刺激反应不佳，来自这只眼睛的丘脑输入最终被撤回。虽然这种重塑被认为是在皮层第4层的丘脑皮质突触开始的，但最近的实验表明，生理可塑性在核上层比皮层第4层进行得更早。这些发现提示了一种可能性，即丘脑皮层重组是由皮层内连接的早期变化所引导的。然而，目前尚不清楚是什么类型的皮质回路改变导致了核上层的快速可塑性。为了解决这个问题，本研究旨在探索从第4层到第3层的皮质内上行轴突的形态可塑性，这给核上细胞提供了强烈的兴奋输入。我们还检查了皮层中神经营养因子的含量，它在神经突延伸中起作用。固有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III层。通过在MD前后同一位置注射两种逆行示踪剂，我们检测了标记IV层细胞分布与眼优势柱模式的可能变化。部分病例MD后剥夺眼柱内标记细胞数量减少。MD还能降低视皮层脑源性神经营养因子蛋白水平。这些结果表明，MD可能会诱导服务于被剥夺眼睛的皮质内轴突的收缩，而BDNF可能有助于收缩。

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.