Developmental nicotine exposure disrupts dendritic arborization patterns of hypoglossal motoneurons in the neonatal rat.
Developmental nicotine exposure disrupts dendritic arborization patterns of hypoglossal motoneurons in the neonatal rat.
复制标题
发育过程中的尼古丁暴露会破坏新生大鼠舌下运动神经元的树突状树枝化模式。
DOI：
10.1002/dneu.22379
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发表时间：
2016
影响因子：
3
通讯作者：
Levine,RichardB
中科院分区：
文献类型：
--
作者：
Powell,GregoryL;Gaddy,Joshua;Xu,Fei;Fregosi,RalphF;Levine,RichardB
母亲在怀孕期间吸烟或使用其他含有尼古丁的产品可能会对新生儿的呼吸功能产生严重的不良后果。我们在之前的研究中已经表明，模型系统中的发育性尼古丁暴露（DNE）会损害脑干内呼吸回路的正常功能。 DNE 的影响包括神经支配舌头肌肉的舌下运动神经元的兴奋性和突触相互作用的改变。本研究旨在检验以下假设：DNE 的这些功能后果伴随着舌下运动神经元树突形态的变化。在全细胞膜片钳记录期间，脑干切片中的舌下运动神经元充满神经生物素，并进行组织学处理以显示树突。形态计量分析（包括 Sholl 方法）揭示了 DNE 对树突分支模式的显着影响。特别是，在出生后的前五天内，对照动物的运动神经元的高阶树突状分支显着生长，而接受 DNE 的新生儿的运动神经元的生长受到损害。 © 2016 Wiley periodicals, Inc. 开发 Neurobiol 76: 1125–1137, 2016
Maternal smoking or use of other products containing nicotine during pregnancy can have significant adverse consequences for respiratory function in neonates. We have shown, in previous studies, that developmental nicotine exposure (DNE) in a model system compromises the normal function of respiratory circuits within the brainstem. The effects of DNE include alterations in the excitability and synaptic interactions of the hypoglossal motoneurons, which innervate muscles of the tongue. This study was undertaken to test the hypothesis that these functional consequences of DNE are accompanied by changes in the dendritic morphology of hypoglossal motoneurons. Hypoglossal motoneurons in brain stem slices were filled with neurobiotin during whole‐cell patch clamp recordings and subjected to histological processing to reveal dendrites. Morphometric analysis, including the Sholl method, revealed significant effects of DNE on dendritic branching patterns. In particular, whereas within the first five postnatal days there was significant growth of the higher‐order dendritic branches of motoneurons from control animals, the growth was compromised in motoneurons from neonates that were subjected to DNE. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 76: 1125–1137, 2016