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Oxytocin modulates respiratory heart rate variability through a hypothalamus–brainstem–heart neuronal pathway.

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Title: Oxytocin modulates respiratory heart rate variability through a hypothalamus–brainstem–heart neuronal pathway.
Authors: Buron, Julie (AUTHOR), Linossier, Ambre (AUTHOR), Gestreau, Christian (AUTHOR), Schaller, Fabienne (AUTHOR), Tyzio, Roman (AUTHOR), Felix, Marie-Solenne (AUTHOR), Matarazzo, Valéry (AUTHOR), Thoby-Brisson, Muriel (AUTHOR), Muscatelli, Françoise (AUTHOR), Menuet, Clément (AUTHOR)
Source: Nature Neuroscience. Nov2025, Vol. 28 Issue 11, p2247-2261. 15p.
Abstract: The variation in heart rate in phase with breathing is called respiratory heart rate variability (RespHRV). Relaxation and positive socio-emotional states can amplify RespHRV, yet the underlying mechanism remains largely unknown. Here we identify a hypothalamus–brainstem neuronal pathway in rodents through which oxytocin (OT) amplifies RespHRV during calming behavior. OT neurons from the caudal paraventricular nucleus in the hypothalamus regulate the activity of a subgroup of inhibitory neurons in the pre-Bötzinger complex, the brainstem nucleus that generates the inspiratory rhythm. Specifically, OT enhances the glycinergic input from OT-receptor-expressing neurons in the pre-Bötzinger complex to cardiac-innervating parasympathetic neurons in the nucleus ambiguus during inspiration. This leads to amplified respiratory modulation of parasympathetic activity to the heart, thereby enhancing RespHRV. We show that OT neurons participate in the restoration of RespHRV amplitude during recovery from stress in mice, indicating that OT acts centrally to regulate cardiac activity during a calming behavior. Buron et al. show that oxytocin enhances heart rate variability linked to breathing during recovery from stress. This calming and cardio-protective effect is produced through a hypothalamus–brainstem pathway for parasympathetic control of the heart. [ABSTRACT FROM AUTHOR]
Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Oxytocin modulates respiratory heart rate variability through a hypothalamus–brainstem–heart neuronal pathway.
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  Data: <searchLink fieldCode="JN" term="%22Nature+Neuroscience%22">Nature Neuroscience</searchLink>. Nov2025, Vol. 28 Issue 11, p2247-2261. 15p.
– Name: Abstract
  Label: Abstract
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  Data: The variation in heart rate in phase with breathing is called respiratory heart rate variability (RespHRV). Relaxation and positive socio-emotional states can amplify RespHRV, yet the underlying mechanism remains largely unknown. Here we identify a hypothalamus–brainstem neuronal pathway in rodents through which oxytocin (OT) amplifies RespHRV during calming behavior. OT neurons from the caudal paraventricular nucleus in the hypothalamus regulate the activity of a subgroup of inhibitory neurons in the pre-Bötzinger complex, the brainstem nucleus that generates the inspiratory rhythm. Specifically, OT enhances the glycinergic input from OT-receptor-expressing neurons in the pre-Bötzinger complex to cardiac-innervating parasympathetic neurons in the nucleus ambiguus during inspiration. This leads to amplified respiratory modulation of parasympathetic activity to the heart, thereby enhancing RespHRV. We show that OT neurons participate in the restoration of RespHRV amplitude during recovery from stress in mice, indicating that OT acts centrally to regulate cardiac activity during a calming behavior. Buron et al. show that oxytocin enhances heart rate variability linked to breathing during recovery from stress. This calming and cardio-protective effect is produced through a hypothalamus–brainstem pathway for parasympathetic control of the heart. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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