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去传入神经支配在听力开始后会在听觉脑干中诱导出新的轴突投射。

Deafferentation induces novel axonal projections in the auditory brainstem after hearing onset.

作者信息

Hsieh Candace Y, Cramer Karina S

机构信息

Department of Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697-4550, USA.

出版信息

J Comp Neurol. 2006 Aug 1;497(4):589-99. doi: 10.1002/cne.21002.

DOI:10.1002/cne.21002
PMID:16739167
Abstract

Deafferentation of neural tissue can result in cell death, morphological changes, and/or alterations in sources of innervation. These changes often occur during a limited period of development. In the auditory brainstem, the ventral cochlear nucleus (VCN) projects to the contralateral but not ipsilateral medial nucleus of the trapezoid body (MNTB). This pathway is part of a circuit that computes interaural intensity differences used in sound localization. Previous studies have shown that, after the cochlea is removed early in postnatal development, cells in the VCN on the deafferented side die, and the intact VCN innervates MNTB on both sides of the brain. These changes after cochlea removal are limited to an early postnatal period that preceeds hearing onset. In this study, we lesioned the VCN directly to evaluate plasticity in axonal pathways after hearing onset. We found that novel projections from the intact VCN to ipsilateral MNTB emerge after lesions performed as late as postnatal day 25. The morphological sequence of events is similar to that seen during the initial development of this pathway. These data suggest that plasticity in the auditory brainstem is possible when pathways are challenged with denervation of target nuclei. The results show that the opportunity for plasticity in auditory brainstem circuitry is more prolonged than previously thought and that novel pathways can form after the normal pathways are fully mature and functional. Moreover, sensitive periods for changes in individual pathways are independently regulated.

摘要

神经组织的传入神经切断可导致细胞死亡、形态变化和/或神经支配来源的改变。这些变化通常发生在有限的发育时期。在听觉脑干中,腹侧耳蜗核(VCN)投射到对侧而非同侧的梯形体内侧核(MNTB)。该通路是用于声音定位的双耳强度差计算回路的一部分。先前的研究表明,在出生后早期去除耳蜗后,去传入侧的VCN中的细胞死亡,而完整的VCN支配脑两侧的MNTB。去除耳蜗后的这些变化仅限于听力开始前的早期出生后阶段。在本研究中,我们直接损伤VCN以评估听力开始后轴突通路的可塑性。我们发现,在出生后第25天这么晚进行损伤后,可以出现从完整的VCN到同侧MNTB的新投射。事件的形态学序列与该通路最初发育期间所见的相似。这些数据表明,当通路因靶核去神经支配而受到挑战时,听觉脑干中的可塑性是可能的。结果表明,听觉脑干回路中可塑性的机会比以前认为的更长,并且在正常通路完全成熟并发挥功能后可以形成新的通路。此外,各个通路变化的敏感期是独立调节的。

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