Using the rhythmic brainstem slice preparation, which contains the preBötzinger complex (preBötC) and the hypoglossal nucleus, we tested the hypothesis that central HO-2 dysregulation weakens hypoglossal motoneuron output. Disrupting HO-2 activity increased transmission failure as determined by the intermittent inability of the preBötC rhythm to trigger output from the hypoglossal nucleus.  Failed transmission was associated with a reduced input-output relationship between the preBötC and the motor nucleus.  These network phenomena were related to smaller inspiratory drive currents and reduced intrinsic excitability among hypoglossal neurons. In addition to HO-2, hypoglossal neurons also expressed the CO-regulated H2S producing enzyme cystathionine ϒ-lyase (CSE). H2S abundance was higher in hypoglossal neurons of HO-2 null mice than wild-type controls. Disrupting CSE function normalized transmission in HO-2 null mice and an H2S donor mimicked the effects of HO-2 dysregulation. These findings demonstrate a hitherto uncharacterized modulation of hypoglossal activity through the interaction of HO‑2 and CSE-derived H2S, and supports the perspective that centrally derived HO-2 activity plays an important role regulating upper airway control. This archived dataset contains the numerical data used to generate the figures in the preprint titled:  Gasotransmitter Modulation of Hypoglossal Motoneuron Activity by Brigitte Browe, Ying-Jie Peng, Jayasri Nanduri, Nanduri R. Prabhakar, and Alfredo J. Garcia III. This report can be found at https://www.biorxiv.org/content/10.1101/2022.03.23.485481. 

These data were collected from electrophysiological measurements.  Data was analyzed posthoc using CLAMPFIT, a part of the pCLAMP software suite (Molecular Devices).  Numerical values were generated using spreadsheet calculations in Excel (Microsoft). The resulting values were aggregated in a single summary file for each figure.  

Data is archived in a Microsoft Excel format.