Exaggerated potassium current reduction by oxytocin in visceral sensory neurons following chronic intermittent hypoxia.
Autor: | Dantzler HA; Department of Biomedical Sciences, Dalton Cardiovascular Research Center, University of Missouri, 134 Research Park Dr., Columbia, MO 65211, USA. Electronic address: dantzlerh@missouri.edu., Kline DD; Department of Biomedical Sciences, Dalton Cardiovascular Research Center, University of Missouri, 134 Research Park Dr., Columbia, MO 65211, USA. Electronic address: klinedd@missouri.edu. |
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Jazyk: | angličtina |
Zdroj: | Autonomic neuroscience : basic & clinical [Auton Neurosci] 2020 Dec; Vol. 229, pp. 102735. Date of Electronic Publication: 2020 Sep 28. |
DOI: | 10.1016/j.autneu.2020.102735 |
Abstrakt: | Oxytocin (OT) from the hypothalamus is increased in several cardiorespiratory nuclei and systemically in response to a variety of stimuli and stressors, including hypoxia. Within the nucleus tractus solitarii (nTS), the first integration site for cardiorespiratory reflexes, OT enhances synaptic transmission, action potential (AP) discharge, and cardiac baroreflex gain. The hypoxic stressor obstructive sleep apnea, and its CIH animal model, elevates blood pressure and alters heart rate variability. The nTS receives sensory input from baroafferent neurons that originate in the nodose ganglia. Nodose neurons express the OT receptor (OTR) whose activation elevates intracellular calcium. However, the influence of OT on other ion channels, especially potassium channels important for neuronal activity during CIH, is less known. This study sought to determine the mechanism (s) by which OT modulates sensory afferent-nTS mediated reflexes normally and after CIH. Nodose ganglia neurons from male Sprague-Dawley rats were examined after 10d CIH (6% O (Copyright © 2020 Elsevier B.V. All rights reserved.) |
Databáze: | MEDLINE |
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