Funke Frank, Müller Michael, Dutschmann Mathias
DFG Research Center Molecular Physiology of the Brain, Zentrum für Physiologie und Pathophysiologie, Georg-August-Universität Göttingen, Humboldtallee 23, 37073, Göttingen, Germany.
Pflugers Arch. 2008 Oct;457(1):185-95. doi: 10.1007/s00424-008-0509-2. Epub 2008 May 6.
Recent studies showed that respiratory rhythm generation depends on oscillators located in the pre-Bötzinger complex (pre-BötC) and the parafacial respiratory group (pFRG). To study inhibitory synaptic interactions between these two oscillators, we developed a rostrally tilted transversal slice preparation, which preserves these regions. The onset of rhythmic mass activity in the retrotrapezoid nucleus (RTN)/pFRG preceded that of the pre-BötC. Blockade of glycinergic and gamma-aminobutyric acidic inhibition synchronized pre-BötC and RTN/pFRG activity and significantly increased pre-BötC burst frequency, amplitude, and duration. Population imaging revealed recruitment of inspiratory-like neurones, while expiratory-like neurones lost their phasic activity. The reconfiguration after disinhibition reveals: (1) synaptic inhibition of the pre-BötC arising from the RTN/pFRG, (2) excitatory drive from the RTN/pFRG that triggers the pre-BötC burst. Our findings support the view that these synaptic interactions in vitro relate to the initiation of the inspiratory phase or to the steering of the expiratory-inspiratory phase transition in vivo.
最近的研究表明，呼吸节律的产生依赖于位于前包钦格复合体（pre-BötC）和面神经旁呼吸组（pFRG）的振荡器。为了研究这两个振荡器之间的抑制性突触相互作用，我们开发了一种向前倾斜的横向切片制备方法，该方法保留了这些区域。后梯形核（RTN）/pFRG中节律性群体活动的起始先于pre-BötC。甘氨酸能和γ-氨基丁酸抑制的阻断使pre-BötC和RTN/pFRG活动同步，并显著增加了pre-BötC的爆发频率、幅度和持续时间。群体成像显示吸气样神经元被募集，而呼气样神经元失去了其相位活动。去抑制后的重构揭示了：（1）RTN/pFRG对pre-BötC的突触抑制，（2）RTN/pFRG触发pre-BötC爆发的兴奋性驱动。我们的研究结果支持这样一种观点，即这些体外的突触相互作用与吸气相的起始或体内呼气-吸气相转换的调控有关。
