ArticleThe Journal of physiology2024
Oxytocin and corticotropin-releasing hormone exaggerate nucleus tractus solitarii neuronal and synaptic activity following chronic intermittent hypoxia.
Article in The Journal of physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Molecular changes in hypoxia-induced central neural circuits and nuclei.Medical gas research · 2026Review
- Exercise-induced neuropeptidergic and neurochemical neuroadaptation in stress regulation and emotional disorders.Acta neurologica Belgica · 2026Review
- From Molecules to Meaning: Integrating Neuropeptides, Sociostasis, and Hormesis in the Brain-Heart Axis.Current issues in molecular biology · 2026Review
- Cardiac vagal motor neurons.Current opinion in neurobiology · 2025Review
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4 authors.
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Abstract
Chronic intermittent hypoxia (CIH) in rodents mimics the hypoxia-induced elevation of blood pressure seen in individuals experiencing episodic breathing. The brainstem nucleus tractus solitarii (nTS) is the first site of visceral sensory afferent integration, and thus is critical for cardiorespiratory homeostasis and its adaptation during a variety of stressors. In addition, the paraventricular nucleus of the hypothalamus (PVN), in part through its nTS projections that contain oxytocin (OT) and/or corticotropin-releasing hormone (CRH), contributes to cardiorespiratory regulation. Within the nTS, these PVN-derived neuropeptides alter nTS activity and the cardiorespiratory response to hypoxia. Nevertheless, their contribution to nTS activity after CIH is not fully understood. We hypothesized that OT and CRH would increase nTS activity to a greater extent following CIH, and co-activation of OT+CRH receptors would further magnify nTS activity. Our data show that compared to their normoxic controls, 10 days' CIH exaggerated nTS discharge, excitatory synaptic currents and Ca
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