ArticleFrontiers in neural circuits2013
β-Noradrenergic receptor activation specifically modulates the generation of sighs in vivo and in vitro.
Article in Frontiers in neural circuits, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 39 citations in OpenAlex.
- Astrocyte activation in the ventrolateral medulla modulates breathing and arousal states.Nature communications · 2026Article
- Sighs Shape Respiratory Variability and Pupil Dynamics and Adapt to Sustained Attention Demands.Psychophysiology · 2026Article
- Inspiratory and sigh breathing rhythms depend on distinct cellular signalling mechanisms in the preBötzinger complex.The Journal of physiology · 2024Article
- Brainstem astrocytes regulate breathing and may affect arousal state in rats.Physiology & behavior · 2024Article
- A comparative examination of morphine and fentanyl: unravelling the differential impacts on breathing and airway stability.The Journal of physiology · 2023Article
- Purinergic signaling mediates neuroglial interactions to modulate sighs.Nature communications · 2023Article
- The astrocytic NaThe Journal of physiology · 2023Article
- The psychophysiology of the sigh: I: The sigh from the physiological perspective.Biological psychology · 2022Review
- The sigh and related behaviors.Handbook of clinical neurology · 2022Review
- Differential Contribution of the Retrotrapezoid Nucleus and C1 Neurons to Active Expiration and Arousal in Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Breathing responses produced by optogenetic stimulation of adrenergic C1 neurons are dependent on the connection with preBötzinger complex in rats.Pflugers Archiv : European journal of physiology · 2018Article
- Locus Coeruleus as a vigilance centre for active inspiration and expiration in rats.Scientific reports · 2018Article
- Defining the Rhythmogenic Elements of Mammalian Breathing.Physiology (Bethesda, Md.) · 2018Review
- Impaired chemosensory control of breathing after depletion of bulbospinal catecholaminergic neurons in rats.Pflugers Archiv : European journal of physiology · 2018Article
- Effects on breathing of agonists to μ-opioid or GABARespiratory physiology & neurobiology · 2017Article
- Chronic Intermittent Hypoxia Differentially Impacts Different States of Inspiratory Activity at the Level of the preBötzinger Complex.Frontiers in physiology · 2017Article
- Activation of β-noradrenergic receptors enhances rhythmic bursting in mouse olfactory bulb external tufted cells.Journal of neurophysiology · 2016Article
- Growth restriction induced by chronic prenatal hypoxia affects breathing rhythm and its pontine catecholaminergic modulation.Journal of neurophysiology · 2016Article
- In vitro characterization of noradrenergic modulation of chemosensitive neurons in the retrotrapezoid nucleus.Journal of neurophysiology · 2016Article
- Locus Ceruleus Norepinephrine Release: A Central Regulator of CNS Spatio-Temporal Activation?Frontiers in synaptic neuroscience · 2016Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The pre-Bötzinger complex (preBötC), an area that is critical for generating breathing (eupnea), gasps and sighs is continuously modulated by catecholamines. These amines and the generation of sighs have also been implicated in the regulation of arousal. Here we studied the catecholaminergic modulation of sighs not only in anesthetized freely breathing mice (in vivo), but also in medullary slice preparations that contain the preBötC and that generate fictive eupneic and sigh rhythms in vitro. We demonstrate that activating β-noradrenergic receptors (β-NR) specifically increases the frequency of sighs, while eupnea remains unaffected both in vitro and in vivo. β-NR activation specifically increased the frequency of intrinsically bursting pacemaker neurons that rely on persistent sodium current (I(Nap)). By contrast, all parameters of bursting pacemakers that rely on the non-specific cation current (I(CAN)) remained unaffected. Moreover, riluzole, which blocks bursting in I(Nap) pacemakers abolished sighs altogether, while flufenamic acid (FFA) which blocks the I(CAN) current did not alter the sigh-increasing effect caused by β-NR. Our results suggest that the selective β-NR action of sighs may result from the modulation of I(Nap) pacemaker activity and that disturbances in noradrenergic system may contribute to abnormal arousal response. The β-NR action on the preBötC may be an important mechanism in modulating behaviors that are specifically associated with sighs, such as the regulation of the early events leading to the arousal response.
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