Molecular Visual Plasticity Group, Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences, Amsterdam, The Netherlands.
Nat Neurosci. 2010 May;13(5):642-8. doi: 10.1038/nn.2534. Epub 2010 Apr 18.
During development and aging and in amblyopia, visual acuity is far below the limitations set by the retina. Expression of brain-derived neurotrophic factor (BDNF) in the visual cortex is reduced in these situations. We asked whether neurotrophic tyrosine kinase receptor, type 2 (TrkB) regulates cortical visual acuity in adult mice. We found that genetically interfering with TrkB/BDNF signaling in pyramidal cells in the mature visual cortex reduced synaptic strength and resulted in a loss of neural responses to high spatial-frequency stimuli. Responses to low spatial-frequency stimuli were unaffected. This selective loss was not accompanied by a change in receptive field sizes or plasticity, but apparent contrast was reduced. Our results indicate that a dependence on spatial frequency in the Heeger normalization model explains this selective effect of contrast reduction on high-resolution vision and suggest that it involves contrast gain control operating in the visual cortex.
在发育、衰老和弱视过程中，视力远低于视网膜的限制。在这些情况下，大脑源性神经营养因子 (BDNF) 在视皮层中的表达减少。我们想知道神经营养酪氨酸激酶受体 2（TrkB）是否调节成年小鼠的皮质视觉敏锐度。我们发现，在成熟视皮层的锥体神经元中，基因干扰 TrkB/BDNF 信号会降低突触强度，并导致对高空间频率刺激的神经反应丧失。而对低空间频率刺激的反应不受影响。这种选择性丧失并不伴有感受野大小或可塑性的变化，而是明显的对比度降低。我们的结果表明，在 Heeger 归一化模型中对空间频率的依赖性解释了这种对比度降低对高分辨率视觉的选择性影响，并表明它涉及在视皮层中运行的对比度增益控制。
