Plasticity of cortical neurons in the developing visual cortex.

哺乳动物新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。单眼剥夺（MD）在出生后早期的生活重塑的初级视觉皮层的神经回路，使大多数神经元反应不良的刺激呈现给剥夺的眼睛和丘脑输入从这只眼睛最终收回。虽然这种重塑已被认为是启动在丘脑皮层突触在皮层第四层，最近的实验表明，生理可塑性进行更早的颗粒层比第四层的皮质。这些研究结果表明，丘脑皮质重组的可能性，指导早期变化的皮质内连接。然而，它仍然是未知的是什么类型的修改，在皮层电路的基础上，这种快速可塑性在颗粒层。为了解决这个问题，本研究的目的是探讨形态可塑性的皮质内上行轴突从第IV层到第III层，给强烈的兴奋性输入颗粒上细胞。此外，我们还研究了皮质神经营养因子的含量，这些神经营养因子在神经突延伸中发挥作用。光学成像的内在信号，使我们能够确定眼优势柱，并注入逆行示踪剂inlayer III的眼优势柱的边界。通过注射两个逆行示踪剂在相同的位置之前和之后的MD，我们研究了可能的变化，标记层IV细胞的分布与眼优势柱模式。在某些情况下，MD后剥夺眼柱中的标记细胞数量减少。MD还降低视皮层脑源性神经营养因子的蛋白水平。这些结果表明，MD可能会引起收缩的皮质内轴突服务的剥夺眼睛和BDNF可能有助于回缩。

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.