CONDITIONING LESIONS ENHANCE GROWTH STATE ONLY IN SENSORY NEURONS LACKING CALCITONIN GENE-RELATED PEPTIDE AND ISOLECTIN B4-BINDING
CONDITIONING LESIONS ENHANCE GROWTH STATE ONLY IN SENSORY NEURONS LACKING CALCITONIN GENE-RELATED PEPTIDE AND ISOLECTIN B4-BINDING
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DOI：
10.1016/j.neuroscience.2009.12.019
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发表时间：
2010-03-10
期刊：
影响因子：
3.3
通讯作者：
Keast, J. R.
中科院分区：
文献类型：
--
作者：
Kalous, A.;Keast, J. R.
调理损伤可通过增强内在生长能力来改善后续损伤后背根神经节 (DRG) 神经元的中央和外周轴突的再生。这种增强的生长状态也在培养的 DRG 神经元中观察到，这些神经元在体内先前的调理损伤后支持更稀疏和快速伸长的生长模式。在这里，我们研究了特定类型感觉神经元再生生长的能力或要求的差异，这对于制定改善损伤后恢复的策略具有重要影响。我们发现，在小鼠坐骨神经部分或完全损伤后，仅在不表达降钙素基因相关肽（CGRP）或结合单叶班代拉菌 I-异凝集素 B4（IB4）的 DRG 神经元中激活体外生长模式。我们还直接检查了条件感觉神经元对神经生长因子（NGF）的反应，神经生长因子不会增强体内受损周围神经的生长。我们发现，部分损伤后，NGF 刺激高度分支和线性限制的生长模式，而不是伸长模式。完全损伤后，NGF 的功能受损，DRG 的免疫组织化学研究表明，这至少部分是由于 NGF 受体、原肌球蛋白相关激酶 A (TrkA) 的下调所致。这些结果表明，无论调理损伤的类型如何，每种类型的 DRG 神经元都具有独特的内在能力或激活快速伸长生长的要求，这似乎不受 NGF 的影响。 (C) 2010 国际广播组织。由爱思唯尔有限公司出版。保留所有权利。
A conditioning lesion improves regeneration of central and peripheral axons of dorsal root ganglion (DRG) neurons after a subsequent injury by enhancing intrinsic growth capacity. This enhanced growth state is also observed in cultured DRG neurons, which support a more sparsely and rapidly elongating mode of growth after a prior conditioning lesion in vivo. Here we examined differences in the capacity or requirements of specific types of sensory neurons for regenerative growth, which has important consequences for development of strategies to improve recovery after injury. We showed that after partial or complete injury of the sciatic nerve in mice, an elongating mode of growth in vitro was activated only in DRG neurons that did not express calcitonin gene-related peptide (CGRP) or bind Bandeiraea simplicifolia I-isolectin B4 (IB4). We also directly examined the response of conditioned sensory neurons to nerve growth factor (NGF), which does not enhance growth in injured peripheral nerves in vivo. We showed that after partial injury, NGF stimulated a highly branched and linearly restricted rather than elongating mode of growth. After complete injury, the function of NGF was impaired, which immunohistochemical studies of DRG indicated was at least partly due to downregulation of the NGF receptor, tropomyosin-related kinase A (TrkA). These results suggest that, regardless of the type of conditioning lesion, each type of DRG neuron has a distinct intrinsic capacity or requirement for the activation of rapidly elongating growth, which does not appear to be influenced by NGF. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.