Department of Applied Science, Integrated Science Center, William & Mary, Williamsburg, VA 23185.
Department of Applied Science, Integrated Science Center, William & Mary, Williamsburg, VA 23185
eNeuro. 2020 Jun 12;7(3). doi: 10.1523/ENEURO.0302-19.2020. Print 2020 May/Jun.
The preBötzinger complex (preBötC) gives rise to two types of breathing behavior under normal physiological conditions: eupnea and sighing. Here, we examine the neural mechanisms that couple their underlying rhythms. We measured breathing in awake intact adult mice and recorded inspiratory rhythms from the preBötC in neonatal mouse brainstem slice preparations. We show previously undocumented variability in the temporal relationship between sigh breaths or bursts and their preceding eupneic breaths or inspiratory bursts. Investigating the synaptic mechanisms for this variability , we further show that pharmacological blockade of chloride-mediated synaptic inhibition strengthens inspiratory-to-sigh temporal coupling. These findings contrast with previous literature, which suggested glycinergic inhibition linked sigh bursts to their preceding inspiratory bursts with minimal time intervals. Furthermore, we verify that pharmacological disinhibition did not alter the duration of the prolonged interval that follows a sigh burst before resumption of the inspiratory rhythm. These results demonstrate that synaptic inhibition does not enhance coupling between sighs and preceding inspiratory events or contribute to post-sigh apneas. Instead, we conclude that excitatory synaptic mechanisms coordinate inspiratory (eupnea) and sigh rhythms.
在正常生理条件下，前脑桥呼吸复合体（preBötC）产生两种呼吸行为：平和呼吸和叹息。在这里，我们研究了连接它们潜在节律的神经机制。我们在清醒的完整成年小鼠中测量呼吸，并在新生小鼠脑片制备中记录 preBötC 的吸气节律。我们展示了以前未记录到的叹息呼吸或爆发与其前导的平和呼吸或吸气爆发之间的时间关系的可变性。研究这种可变性的突触机制，我们进一步表明，氯介导的突触抑制的药理学阻断增强了吸气到叹息的时间耦合。这些发现与以前的文献形成对比，以前的文献表明甘氨酸能抑制将叹息爆发与其前导的吸气爆发联系起来，时间间隔最小。此外，我们验证了药理学去抑制并没有改变叹息爆发后恢复吸气节律之前延长间隔的持续时间。这些结果表明，突触抑制不会增强叹息和前导吸气事件之间的耦合，也不会导致叹息后呼吸暂停。相反，我们得出结论，兴奋性突触机制协调吸气（平和呼吸）和叹息节律。
