Lee Kun-Ze, Fuller David D
Department of Physical Therapy, University of Florida, College of Public Health and Health Professions, McKnight Brain Institute, PO Box 100154, 100 Newell Dr, Gainesville, FL 32610, USA.
J Appl Physiol (1985). 2010 May;108(5):1187-98. doi: 10.1152/japplphysiol.01285.2009. Epub 2010 Feb 11.
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 (PaO2 of approximately 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.
舌下神经（Ⅻ）与呼吸相关的放电由吸气前（Pre-I）和吸气（I）活动组成。我们的首要目的是检验以下假设：低氧诱导的Ⅻ运动输出可塑性在Pre-I与I期Ⅻ爆发中存在差异表达。在氨基甲酸乙酯麻醉、迷走神经切断并通气的大鼠中，通过暴露于等容性低氧（动脉血氧分压约为35托）诱导Ⅻ运动输出的短期增强（STP）。在低氧开始时，Pre-I和I期Ⅻ放电均突然增加（即急性低氧反应），Pre-I期放电幅度的相对增加（相对于基线为507±46%）远大于I期爆发（相对于基线为257±16%；P<0.01）。此外，低氧后STP在I期爆发中表达，但Pre-I期爆发中未表达。具体而言，低氧终止后I期活动仍保持升高，但Pre-I期爆发突然恢复到低氧前水平。我们的第二个目的是检验以下假设：I期Ⅻ活动的STP是由于募集了不活动或“沉默”的Ⅻ运动神经元（MNs），还是由于活动MNs的速率编码。基于基线放电模式，使用单纤维记录将Ⅻ MNs分类为I型、呼气-吸气型或沉默型。低氧后I期Ⅻ活动的STP与活动I型和沉默MNs放电频率增加有关，但与呼气-吸气型MNs无关。我们得出结论，呼吸可塑性的表达在Pre-I和I期Ⅻ活动之间受到差异调节。此外，沉默MNs的募集和活动I型MNs的速率编码均有助于低氧后Ⅻ运动输出的增加。
