Preinspiratory and inspiratory hypoglossal motor output during hypoxia-induced plasticity in the rat
Preinspiratory and inspiratory hypoglossal motor output during hypoxia-induced plasticity in the rat
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DOI：
10.1152/japplphysiol.01285.2009
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发表时间：
2010-05-01
影响因子：
3.3
通讯作者：
Fuller, David D.
中科院分区：
文献类型：
--
作者：
Lee, Kun-Ze;Fuller, David D.
李 K-Z，富勒 DD。缺氧诱导的大鼠可塑性期间吸气前和吸气舌下运动输出。 J Appl Physiol 108: 1187-1198, 2010。首次发表于 2010 年 2 月 11 日； doi:10.1152/japplphyol.01285.2009.-舌下 (XII) 神经中与呼吸相关的放电由吸气前 (pre-I) 和吸气 (I) 活动组成。我们的第一个目的是测试以下假设：缺氧诱导的 XII 运动输出可塑性在 I 前与 I XII 爆发中表达存在差异。在氨基甲酸乙酯麻醉、迷走神经切断和通气的大鼠中，通过暴露于等二氧化碳缺氧（Pa(O2) 类似于 35 Torr），诱导 XII 运动输出的短期增强 (STP)。 I 前和 I XII 放电在缺氧开始时（即急性缺氧反应）突然增加，并且 I 前（507 +/- 46% 基线）与 I 爆发（257 +/- 16% 基线；P < 0.01）相比，振幅的相对增加要大得多。此外，STP 在 I 中表达，但在缺氧后 I 爆发前不表达。具体而言，缺氧终止后 I 活性保持升高，但 I 爆发前突然恢复到缺氧前水平。我们的第二个目的是测试以下假设：IXI 活性的 STP 是由不活跃或“沉默”XII 运动神经元 (MN) 的募集与活跃 MN 的速率编码引起的。单纤维记录用于根据基线放电模式将 XII MN 分类为 I、呼气-吸气或无声。缺氧后 I XII 活性的 STP 与活动 I 和沉默 MN 中的放电频率增加相关，但与呼气-吸气 MN 中无关。我们得出结论，呼吸可塑性的表达在 pre-I 和 IXII 活性之间受到差异性调节。此外，沉默 MN 的募集和活性 I MN 的速率编码都有助于缺氧后 XII 运动输出的增加。
Lee K-Z, Fuller DD. Preinspiratory and inspiratory hypoglossal motor output during hypoxia-induced plasticity in the rat. J Appl Physiol 108: 1187-1198, 2010. First published February 11, 2010; doi:10.1152/japplphysiol.01285.2009.-Respiratory-related discharge in the hypoglossal (XII) nerve is composed of preinspiratory (pre-I) and inspiratory (I) activity. Our first purpose was to test the hypothesis that hypoxia-induced plasticity in XII motor output is differentially expressed in pre-I vs. I XII bursting. Short-term potentiation (STP) of XII motor output was induced in urethane-anesthetized, vagotomized, and ventilated rats by exposure to isocapnic hypoxia (Pa(O2) of similar to 35 Torr). Both pre-I and I XII discharge abruptly increased at beginning of hypoxia (i.e., acute hypoxic response), and the relative increase in amplitude was much greater for pre-I (507 +/- 46% baseline) vs. I bursting (257 +/- 16% baseline; P < 0.01). In addition, STP was expressed in I but not pre-I bursting following hypoxia. Specifically, I activity remained elevated following termination of hypoxia but pre-I bursting abruptly returned to prehypoxia levels. Our second purpose was to test the hypothesis that STP of I XII activity results from recruitment of inactive or "silent" XII motoneurons (MNs) vs. rate coding of active MNs. Single fiber recordings were used to classify XII MNs as I, expiratory-inspiratory, or silent based on baseline discharge patterns. STP of I XII activity following hypoxia was associated with increased discharge frequency in active I and silent MNs but not expiratory-inspiratory MNs. We conclude that the expression of respiratory plasticity is differentially regulated between pre-I and I XII activity. In addition, both recruitment of silent MNs and rate coding of active I MNs contribute to increases in XII motor output following hypoxia.