Division of Physiology, Department of Medicine, University of California, San Diego, USA.
Am J Physiol Regul Integr Comp Physiol. 2011 Aug;301(2):R343-50. doi: 10.1152/ajpregu.00375.2010. Epub 2011 May 18.
During ventilatory acclimatization to hypoxia (VAH), time-dependent increases in ventilation lower Pco(2) levels, and this persists on return to normoxia. We hypothesized that plasticity in the caudal nucleus tractus solitarii (NTS) contributes to VAH, as the NTS receives the first synapse from the carotid body chemoreceptor afferents and also contains CO(2)-sensitive neurons. We lesioned cells in the caudal NTS containing the neurokinin-1 receptor by microinjecting the neurotoxin saporin conjugated to substance P and measured ventilatory responses in awake, unrestrained rats 18 days later. Lesions did not affect hypoxic or hypercapnic ventilatory responses in normoxic control rats, in contrast to published reports for similar lesions in other central chemosensitive areas. Also, lesions did not affect the hypercapnic ventilatory response in chronically hypoxic rats (inspired Po(2) = 90 Torr for 7 days). These results suggest functional differences between central chemoreceptor sites. However, lesions significantly increased ventilation in normoxia or acute hypoxia in chronically hypoxic rats. Hence, chronic hypoxia increases an inhibitory effect of neurokinin-1 receptor neurons in the NTS on ventilatory drive, indicating that these neurons contribute to plasticity during chronic hypoxia, although such plasticity does not explain VAH.
在通气适应低氧（VAH）期间，通气的时间依赖性增加会降低 Pco（2）水平，并且在返回正常氧合时仍然如此。我们假设尾端孤束核（NTS）中的可塑性有助于 VAH，因为 NTS 接收来自颈动脉体化学感受器传入的第一个突触，并且还包含 CO（2）敏感神经元。我们通过将神经毒素 saporin 与 P 物质缀合注入来损伤含有神经激肽-1 受体的尾端 NTS 中的细胞，并在 18 天后测量清醒、未束缚的大鼠的通气反应。与其他中央化学敏感区域的类似损伤的已发表报告相反，损伤不会影响正常氧合对照大鼠的低氧或高碳酸通气反应。此外，损伤也不会影响慢性低氧大鼠的高碳酸通气反应（吸入 Po（2）= 90 托 7 天）。这些结果表明中枢化学感受器部位之间存在功能差异。然而，损伤显著增加了慢性低氧大鼠在正常氧或急性低氧中的通气。因此，慢性低氧增加了 NTS 中神经激肽-1 受体神经元对通气驱动的抑制作用，表明这些神经元有助于慢性低氧期间的可塑性，尽管这种可塑性并不能解释 VAH。
