Cabelli R J, Shelton D L, Segal R A, Shatz C J
Department of Cell and Neurobiology, University of Southern California School of Medicine, Los Angeles 90033, USA.
Neuron. 1997 Jul;19(1):63-76. doi: 10.1016/s0896-6273(00)80348-7.
We have examined the hypothesis that the segregation of LGN axon terminals into ocular dominance (OD) patches in layer 4 of the visual cortex requires neurotrophins, acting as signals to modulate the pattern of synaptic connectivity. Neurotrophin receptor antagonists, composed of the extracellular domain of each member of the trk family of neurotrophin receptors fused to a human Fc domain, were infused directly into visual cortex during the peak phase of OD column formation. Infusion of trkB-IgG, which binds BDNF and NT-4/5, inhibited the formation of OD patches within layer 4, while trkA-IgG and trkC-IgG, which preferentially bind NGF and NT-3, respectively, had no effect. The autoradiographic labeling of LGN terminals in cortical layer 4 was reduced by trkB-IgG, in contrast with the increased labeling observed following NT-4/5 infusion. These data suggest that an endogenous ligand of trkB, normally present in limiting amounts within visual cortex, is necessary for the selective growth and remodeling of LGN axons into eye-specific patches.
我们检验了这样一种假说，即外侧膝状体（LGN）轴突终末在视觉皮层第4层中分离成眼优势（OD）斑块需要神经营养因子，其作为信号来调节突触连接模式。在OD柱形成的高峰期，将由神经营养因子受体trk家族每个成员的细胞外结构域与人Fc结构域融合而成的神经营养因子受体拮抗剂直接注入视觉皮层。结合脑源性神经营因子（BDNF）和神经营养因子-4/5（NT-4/5）的trkB-IgG的注入抑制了第4层内OD斑块的形成，而分别优先结合神经生长因子（NGF）和神经营养因子-3（NT-3）的trkA-IgG和trkC-IgG则没有效果。与注入NT-4/5后观察到的标记增加相反，trkB-IgG减少了皮层第4层中LGN终末的放射自显影标记。这些数据表明，trkB的内源性配体通常以有限的量存在于视觉皮层中，对于LGN轴突选择性生长并重塑为眼特异性斑块是必需的。
