Department of Comparative Biosciences, University of Wisconsin, Madison, WI 53706, USA.
Respir Physiol Neurobiol. 2013 Nov 1;189(2):384-94. doi: 10.1016/j.resp.2013.06.023. Epub 2013 Jun 28.
Multiple forms of plasticity are activated following reduced respiratory neural activity. For example, in ventilated rats, a central neural apnea elicits a rebound increase in phrenic and hypoglossal burst amplitude upon resumption of respiratory neural activity, forms of plasticity called inactivity-induced phrenic and hypoglossal motor facilitation (iPMF and iHMF), respectively. Here, we provide a conceptual framework for plasticity following reduced respiratory neural activity to guide future investigations. We review mechanisms giving rise to iPMF and iHMF, present new data suggesting that inactivity-induced plasticity is observed in inspiratory intercostals (iIMF) and point out gaps in our knowledge. We then survey conditions relevant to human health characterized by reduced respiratory neural activity and discuss evidence that inactivity-induced plasticity is elicited during these conditions. Understanding the physiological impact and circumstances in which inactivity-induced respiratory plasticity is elicited may yield novel insights into the treatment of disorders characterized by reductions in respiratory neural activity.
多种形式的可塑性会在呼吸神经活动减少后被激活。例如，在通气的大鼠中，中枢性神经暂停会导致呼吸神经活动恢复时膈神经和舌下神经爆发幅度的反弹增加，分别称为不活动诱导的膈神经和舌下神经运动易化（iPMF 和 iHMF）。在这里，我们提供了一个关于呼吸神经活动减少后可塑性的概念框架，以指导未来的研究。我们综述了导致 iPMF 和 iHMF 的机制，提出了新的数据表明，不活动诱导的可塑性也存在于吸气肋间肌（iIMF）中，并指出了我们知识中的空白。然后，我们调查了与呼吸神经活动减少相关的人类健康状况，并讨论了在这些情况下引发不活动诱导可塑性的证据。了解不活动诱导呼吸可塑性的生理影响和情况，可能会为治疗以呼吸神经活动减少为特征的疾病提供新的见解。
