EphB2 signaling regulates lesion-induced axon sprouting but not critical period length in the postnatal auditory brainstem.
EphB2 signaling regulates lesion-induced axon sprouting but not critical period length in the postnatal auditory brainstem.
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DOI：
10.1186/1749-8104-8-2
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发表时间：
2013-02-05
影响因子：
3.6
通讯作者：
Cramer KS
中科院分区：
文献类型：
--
作者：
Nakamura PA;Cramer KS
对发育可塑性的研究可以提供对成年期可塑性的深入了解，此时神经回路对输入的损失或变化的反应较低。在哺乳动物听性脑干中，耳蜗腹侧核（VCN）的球状丛状细胞轴突支配对侧斜方体内侧核（MNTB）主神经元。在MNTB的VCN轴突终端，被称为杯，是非常大的，专门用于高保真的听觉信息传输。出生后发育过程中单侧传入神经阻滞后，来自完整侧的VCN轴突与新靶点形成连接，包括同侧MNTB。EphB信号已被证明在这一过程中发挥作用，在出生后的第一周，但在以后的发展时期参与这种重组的机制仍然未知。我们发现，EphB2信号减少诱导的同侧投射到MNTB后，在出生后第七天（P7）单侧VCN去除后，但不是在P10去除一侧VCN后，关闭病变诱导的神经支配的同侧MNTB的关键期后。这项研究的结果表明，参与电路发展的分子机制也可能在发展过程中的去传入神经后的重新布线中发挥作用，但似乎没有调节可塑性的关键时期的长度。
Studies of developmental plasticity may provide insight into plasticity during adulthood, when neural circuitry is less responsive to losses or changes in input. In the mammalian auditory brainstem, globular bushy cell axons of the ventral cochlear nucleus (VCN) innervate the contralateral medial nucleus of the trapezoid body (MNTB) principal neurons. VCN axonal terminations in MNTB, known as calyces of Held, are very large and specialized for high-fidelity transmission of auditory information. Following unilateral deafferentation during postnatal development, VCN axons from the intact side form connections with novel targets, including the ipsilateral MNTB. EphB signaling has been shown to play a role in this process during the first postnatal week, but mechanisms involved in this reorganization during later developmental periods remain unknown. We found that EphB2 signaling reduces the number of induced ipsilateral projections to the MNTB after unilateral VCN removal at postnatal day seven (P7), but not after removal of the VCN on one side at P10, after the closure of the critical period for lesion-induced innervation of the ipsilateral MNTB. Results from this study indicate that molecular mechanisms involved in the development of circuitry may also play a part in rewiring after deafferentation during development, but do not appear to regulate the length of critical periods for plasticity.