Department of Biology and Wildlife, Institute of Arctic Biology, University of Alaska Fairbanks, Fairbanks, Alaska.
Dev Neurobiol. 2010 Sep;70(10):726-35. doi: 10.1002/dneu.20806.
Neuroventilation is highly plastic and exposure to either of two distinct teratogens, nicotine or ethanol, during development results in a similar loss of the neuroventilatory response to hypercapnia in bullfrog tadpoles. Whether this functional deficit is permanent or transient following nicotine or ethanol exposure was unknown. Here, we tested the persistence of hypercapnic neuroventilatory response impairments in tadpoles exposed to either 30 microg/L nicotine or 0.12-0.06 g/dL ethanol for 10 weeks. Brainstem breathing-related neural activity was assessed in tadpoles allowed to develop teratogen-free after either nicotine or ethanol exposure. Nicotine-exposed animals responded normally to hypercapnia after a 3-week teratogen-free period but the hypercapnic response in ethanol-exposed tadpoles remained impaired. Tadpoles allowed to develop for only 1 week nicotine free after chronic exposure were unable to respond to hypercapnia. The hypercapnic response of ethanol-exposed tadpoles returned by 6 weeks following chronic ethanol exposure. These findings suggest that some nicotine- and ethanol-induced impairments can be resolved during early development. Understanding both the disruptive effects of nicotine and ethanol exposure and how impaired responses return when teratogen exposure stops may offer insight on the function and plasticity of respiratory control.
神经通气具有高度的可塑性，在发育过程中暴露于两种不同的致畸剂，尼古丁或乙醇，会导致牛蛙蝌蚪对高碳酸血症的神经通气反应相似的丧失。在尼古丁或乙醇暴露后，这种功能缺陷是永久性的还是暂时性的尚不清楚。在这里，我们测试了暴露于 30 微克/升尼古丁或 0.12-0.06 克/分升乙醇 10 周的蝌蚪中高碳酸血症神经通气反应损伤的持久性。在尼古丁或乙醇暴露后允许无致畸剂发育 3 周后，评估了蝌蚪的脑干呼吸相关神经活动。暴露于尼古丁的动物在无致畸剂的 3 周后对高碳酸血症正常反应，但暴露于乙醇的蝌蚪的高碳酸血症反应仍然受损。在慢性暴露后仅允许发育 1 周无尼古丁的蝌蚪无法对高碳酸血症作出反应。慢性乙醇暴露 6 周后，暴露于乙醇的蝌蚪的高碳酸血症反应恢复。这些发现表明，一些尼古丁和乙醇引起的损伤可以在早期发育过程中得到解决。了解尼古丁和乙醇暴露的破坏作用以及当致畸剂暴露停止时受损反应如何恢复，可能有助于深入了解呼吸控制的功能和可塑性。
