Numerical data from: Gasotransmitter modulation of hypoglossal motoneuron activity
Data files
Feb 07, 2023 version files 546.72 KB
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Figure_1C-_IrSamp_preBotC.xlsx
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Figure_1C-_IrSamp_XIIn.xlsx
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Figure_1D__IO_Ratio_ChrMP.xlsx
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Figure_1D__IO_Ratio_Control.xlsx
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Figure_1E_Transmission_Baseline_ChrMP.xlsx
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Figure_1F-DistributionPreBotCBurstAreaChrMP.xlsx
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Figure_2B_preBotC_IrSamp.xlsx
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Figure_2C_XIIn_IrSamp.xlsx
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Figure_2D_IO_Ratio_HO2ko.xlsx
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Figure_2D_IO_Ratio_WT.xlsx
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Figure_2E-Transmission_WT_HO-2null.xlsx
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Figure_2F-DistributionPreBotCBurstArea.xlsx
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Figure_3B-_preBotC_-_premotor_IO_Ratio_Baseline.xlsx
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Figure_3B-_preBotC_-_premotor_IO_Ratio_ChrMP.xlsx
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Figure_3B-_preBotC-_premotor_Transmission.xlsx
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Figure_3C-_preBotC_-_premotor_IO_Ratio_ChrMP.xlsx
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Figure_3C-_premotor_-_XIIn_Transmission.xlsx
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Figure_4_Supplement_1-_Nonrespiratory_rheobase.xlsx
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Figure_4A-_Drive_Potentials_ChrMP.xlsx
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Figure_4B-_AP_ChrMP.xlsx
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Figure_4C-_Respiratory_Rheobase.xlsx
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Figure_5A-PercentTransmission_of_SubnetworkChrMP.xlsx
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Figure_5B-IrSampChrMP.xlsx
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Figure_6B_H2Sactivity.xlsx
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Figure_6D-_Transmission_NaHS.xlsx
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Figure_6E-_IO_NaHS.xlsx
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Figure_7B_CORM_IO.xlsx
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Figure_7B_Dysreg_HO-2_IO.xlsx
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Figure_7C-_Transmission_CORM-3.xlsx
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Figure_7E_CSE_HO2ko_IO.xlsx
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Figure_7F-_Transmission_HO2-CSE.xlsx
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Figure_8_-Supplement_1-SubnetworkHO2dysregCSE.xlsx
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Figure_8B-LPAG_IO.xlsx
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Figure_8C-LPAG_Transmission.xlsx
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Figure_8E-_Drives_HO-2_LPAG.xlsx
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Figure_9_Supplement1C-__IO_Tolbutamide.xlsx
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Figure_9_Supplement1E-_AP_Tolbutamide.xlsx
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Figure_9-_Supplement1C_Transmission_Tolbutamide.rev1.xlsx
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Figure_9-_Supplement1D-_Drives_Tolbutamide.xlsx
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Figure_9-Supplement1F-_Rheobase_Tolbutamide.xlsx
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Figure_9A-_Drives_ChrMP_Apamin.xlsx
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Figure_9B-_AP_Apamin.xlsx
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Figure_9C-_Rheobase_Apamin.xlsx
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README.docx
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Table1.networkpreBotCXIInproperties.xlsx
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Table2.ChrMPvsHO2.xlsx
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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.
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.