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Numerical data from: Gasotransmitter modulation of hypoglossal motoneuron activity

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Feb 07, 2023 version files 546.72 KB

Abstract

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