Relevant bibliographies by topics / Serotonin, control of breathing

Academic literature on the topic 'Serotonin, control of breathing'

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Published: 10 March 2023

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Journal articles on the topic "Serotonin, control of breathing"

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Kubin, Leszek, Richard O. Davies, and Allan I. Pack. "Control of Upper Airway Motoneurons During REM Sleep." Physiology 13, no. 2 (April 1998): 91–97. http://dx.doi.org/10.1152/physiologyonline.1998.13.2.91.

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The loss of tone in upper airway muscles contributes to disorders of breathing during sleep. In an animal model of rapid eye movement sleep atonia, decrements in the activity of upper airway motoneurons are caused by withdrawal of excitation mediated by serotonin and other transmitters, rather than by state-dependent inhibition.
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Forster, H. V. "Invited Review: Plasticity in the control of breathing following sensory denervation." Journal of Applied Physiology 94, no. 2 (February 1, 2003): 784–94. http://dx.doi.org/10.1152/japplphysiol.00602.2002.

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The purpose of this manuscript is to review the results of studies on the recovery or plasticity following a denervation- or lesion-induced change in breathing. Carotid body denervation (CBD), lung denervation (LD), cervical (CDR) and thoracic (TDR) dorsal rhizotomy, dorsal spinal column lesions, and lesions at pontine, medullary, and spinal sites all chronically alter breathing. The plasticity after these is highly variable, ranging from near complete recovery of the peripheral chemoreflex in rats after CBD to minimal recovery of the Hering-Breuer inflation reflex in ponies after LD. The degree of plasticity varies among the different functions of each pathway, and plasticity varies with the age of the animal when the lesion was made. In addition, plasticity after some lesions varies between species, and plasticity is greater in the awake than in the anesthetized state. Reinnervation is not a common mechanism of plasticity. There is evidence supporting two mechanisms of plasticity. One is through upregulation of an alternate sensory pathway, such as serotonin-mediated aortic chemoreception after CBD. The second is through upregulation on the efferent limb of a reflex, such as serotonin-mediated increased responsiveness of phrenic motoneurons after CDR, TDR, and spinal cord injury. Accordingly, numerous components of the ventilatory control system exhibit plasticity after denervation or lesion-induced changes in breathing; this plasticity is uniform neither in magnitude nor in underlying mechanisms. A major need in future research is to determine whether “reorganization” within the central nervous system contributes to plasticity following lesion-induced changes in breathing.
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Szereda-Przestaszewska, Małgorzata, and Katarzyna Kaczyńska. "Serotonin and substance P: Synergy or competition in the control of breathing." Autonomic Neuroscience 225 (May 2020): 102658. http://dx.doi.org/10.1016/j.autneu.2020.102658.

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Forster, Hubert V. "Julius H. Comroe Distinguished Lecture: Interdependence of neuromodulators in the control of breathing." Journal of Applied Physiology 125, no. 5 (November 1, 2018): 1511–25. http://dx.doi.org/10.1152/japplphysiol.00477.2018.

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In vitro and in vivo anesthetized studies led to the conclusion that “deficiencies in one neuromodulator are immediately compensated by the action of other neuromodulators,” which suggests an interdependence among neuromodulators. This concept was the focus of the 2018 Julius H. Comroe Lecture to the American Physiological Society in which I summarized our published studies testing the hypothesis that if modulatory interdependence was robust, breathing would not decrease during dialysis of antagonists to G protein-coupled excitatory receptors or agonists to inhibitory receptors into the ventral respiratory column (VRC) or the hypoglossal motor nuclei (HMN). We found breathing was not decreased during unilateral VRC dialyses of antagonists to excitatory muscarinic, serotonergic, and neurokinin-1 receptors alone or in combinations nor was breathing decreased with unilateral VRC dialysis of a µ-opioid receptor agonist. Analyses of the effluent dialysate revealed locally increased serotonin (excitatory) during muscarinic receptor blockade and decreased γ-aminobutyric acid (inhibitory) during dialysis of opioid agonists, suggesting an interdependence of neuromodulators through release of compensatory neuromodulators. Bilateral dialysis of receptor antagonists or agonist in the VRC increased breathing, which does not support the concept that unchanged breathing with unilateral dialyses was due to contralateral compensation. In contrast, in the HMN neither unilateral nor bilateral dialysis of the excitatory receptor antagonists altered breathing, but unilateral dialysis of the opioid receptor agonist decreased breathing. We conclude: 1) there is site-dependent interdependence of neuromodulators during physiologic conditions, and 2) attributing physiologic effects to a specific receptor perturbation is complicated by local compensatory mechanisms.
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Ling, Liming, David D. Fuller, Karen B. Bach, Richard Kinkead, E. Burdette Olson, and Gordon S. Mitchell. "Chronic Intermittent Hypoxia Elicits Serotonin-Dependent Plasticity in the Central Neural Control of Breathing." Journal of Neuroscience 21, no. 14 (July 15, 2001): 5381–88. http://dx.doi.org/10.1523/jneurosci.21-14-05381.2001.

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House, John S., Cody E. Nichols, Huiling Li, Christina Brandenberger, Rohan S. Virgincar, Laura M. DeGraff, Bastiaan Driehuys, Darryl C. Zeldin, and Stephanie J. London. "Vagal innervation is required for pulmonary function phenotype in Htr4−/− mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 312, no. 4 (April 1, 2017): L520—L530. http://dx.doi.org/10.1152/ajplung.00495.2016.

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Human genome-wide association studies have identified over 50 loci associated with pulmonary function and related phenotypes, yet follow-up studies to determine causal genes or variants are rare. Single nucleotide polymorphisms in serotonin receptor 4 ( HTR4) are associated with human pulmonary function in genome-wide association studies and follow-up animal work has demonstrated that Htr4 is causally associated with pulmonary function in mice, although the precise mechanisms were not identified. We sought to elucidate the role of neural innervation and pulmonary architecture in the lung phenotype of Htr4−/− animals. We report here that the Htr4−/− phenotype in mouse is dependent on vagal innervation to the lung. Both ex vivo tracheal ring reactivity and in vivo flexiVent pulmonary functional analyses demonstrate that vagotomy abrogates the Htr4−/− airway hyperresponsiveness phenotype. Hyperpolarized 3He gas magnetic resonance imaging and stereological assessment of wild-type and Htr4−/− mice reveal no observable differences in lung volume, inflation characteristics, or pulmonary microarchitecture. Finally, control of breathing experiments reveal substantive differences in baseline breathing characteristics between mice with/without functional HTR4 in breathing frequency, relaxation time, flow rate, minute volume, time of inspiration and expiration and breathing pauses. These results suggest that HTR4’s role in pulmonary function likely relates to neural innervation and control of breathing.
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Yang, Hsiao T., and Kevin J. Cummings. "Brain stem serotonin protects blood pressure in neonatal rats exposed to episodic anoxia." Journal of Applied Physiology 115, no. 12 (December 15, 2013): 1733–41. http://dx.doi.org/10.1152/japplphysiol.00970.2013.

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In neonatal rodents, a loss of brain stem serotonin [5-hydroxytryptamine (5-HT)] in utero or at birth compromises anoxia-induced gasping and the recovery of heart rate (HR) and breathing with reoxygenation (i.e., autoresuscitation). How mean arterial pressure (MAP) is influenced after an acute loss of brain stem 5-HT content is unknown. We hypothesized that a loss of 5-HT for ∼1 day would compromise MAP during episodic anoxia. We injected 6-fluorotryptophan (20 mg/kg ip) into rat pups (postnatal days 9–10 or 11–13, n = 22 treated, 24 control), causing a ∼70% loss of brain stem 5-HT. Pups were exposed to a maximum of 15 anoxic episodes, separated by 5 min of room air to allow autoresuscitation. In younger pups, we measured breathing frequency and tidal volume using “head-out” plethysmography and HR from the electrocardiogram. In older pups, we used whole body plethysmography to detect gasping, while monitoring MAP. Gasp latency and the time required for respiratory, HR, and MAP recovery following each episode were determined. Despite normal gasp latency, breathing frequency and a larger tidal volume ( P < 0.001), 5-HT-deficient pups survived one-half the number of episodes as controls ( P < 0.001). The anoxia-induced decrease in MAP experienced by 5-HT-deficient pups was double that of controls ( P = 0.017), despite the same drop in HR ( P = 0.48). MAP recovery was delayed ∼10 s by 5-HT deficiency ( P = 0.001). Our data suggest a loss of brain stem 5-HT leads to a pronounced, premature loss of MAP in response to episodic anoxia. These data may help explain why some sudden infant death syndrome cases die from what appears to be cardiovascular collapse during apparent severe hypoxia.
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Massey, Cory A., and George B. Richerson. "Isoflurane, ketamine-xylazine, and urethane markedly alter breathing even at subtherapeutic doses." Journal of Neurophysiology 118, no. 4 (October 1, 2017): 2389–401. http://dx.doi.org/10.1152/jn.00350.2017.

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Anesthetics are widely used for animal research on respiratory control in vivo, but their effect on breathing and CO2 chemoreception has not been well characterized in mice, a species now often used for these studies. We previously demonstrated that 1% isoflurane markedly reduces the hypercapnic ventilatory response (HCVR) in adult mice in vivo and masks serotonin [5-hydroxytryptamine (5-HT)] neuron chemosensitivity in vitro. Here we investigated effects of 0.5% isoflurane on breathing in adult mice and also found a large reduction in the HCVR even at this subanesthetic concentration. We then tested the effects on breathing of ketamine-xylazine and urethane, anesthetics widely used in research on breathing. We found that these agents altered baseline breathing and blunted the HCVR at doses within the range typically used experimentally. At lower doses ventilation was decreased, but mice appropriately matched their ventilation to metabolic demands due to a parallel decrease in O2 consumption. Neither ketamine nor urethane decreased chemosensitivity of 5-HT neurons. These results indicate that baseline breathing and/or CO2 chemoreception in mice are decreased by anesthetics widely viewed as not affecting respiratory control, and even at subtherapeutic doses. These effects of anesthetics on breathing may alter the interpretation of studies of respiratory physiology in vivo. NEW & NOTEWORTHY Anesthetics are frequently used in animal research, but their effects on physiological functions in mice have not been well defined. Here we investigated the effects of commonly used anesthetics on breathing in mice. We found that all tested anesthetics significantly reduced the hypercapnic ventilatory response (HCVR), even at subtherapeutic doses. In addition, ketamine-xylazine and urethane anesthesia altered baseline breathing. These data indicate that breathing and the HCVR in mice are highly sensitive to anesthetic modulation.
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Kaplan, Kara, Ashley E. Echert, Ben Massat, Madeleine M. Puissant, Oleg Palygin, Aron M. Geurts, and Matthew R. Hodges. "Chronic central serotonin depletion attenuates ventilation and body temperature in young but not adult Tph2 knockout rats." Journal of Applied Physiology 120, no. 9 (May 1, 2016): 1070–81. http://dx.doi.org/10.1152/japplphysiol.01015.2015.

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Genetic deletion of brain serotonin (5-HT) neurons in mice leads to ventilatory deficits and increased neonatal mortality during development. However, it is unclear if the loss of the 5-HT neurons or the loss of the neurochemical 5-HT led to the observed physiologic deficits. Herein, we generated a mutant rat model with constitutive central nervous system (CNS) 5-HT depletion by mutation of the tryptophan hydroxylase 2 ( Tph2) gene in dark agouti (DA Tph2−/−) rats. DA Tph2−/− rats lacked TPH immunoreactivity and brain 5-HT but retain dopa decarboxylase-expressing raphe neurons. Mutant rats were also smaller, had relatively high mortality (∼50%), and compared with controls had reduced room air ventilation and body temperatures at specific postnatal ages. In adult rats, breathing at rest and hypoxic and hypercapnic chemoreflexes were unaltered in adult male and female DA Tph2−/− rats. Body temperature was also maintained in adult DA Tph2−/− rats exposed to 4°C, indicating unaltered ventilatory and/or thermoregulatory control mechanisms. Finally, DA Tph2−/− rats treated with the 5-HT precursor 5-hydroxytryptophan (5-HTP) partially restored CNS 5-HT and showed increased ventilation ( P < 0.05) at a developmental age when it was otherwise attenuated in the mutants. We conclude that constitutive CNS production of 5-HT is critically important to fundamental homeostatic control systems for breathing and temperature during postnatal development in the rat.
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Dutschmann, M., H. Waki, T. Manzke, A. E. Simms, A. E. Pickering, D. W. Richter, and J. F. R. Paton. "The potency of different serotonergic agonists in counteracting opioid evoked cardiorespiratory disturbances." Philosophical Transactions of the Royal Society B: Biological Sciences 364, no. 1529 (September 12, 2009): 2611–23. http://dx.doi.org/10.1098/rstb.2009.0076.

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Serotonin receptor (5-HTR) agonists that target 5-HT 4(a) R and 5-HT 1A R can reverse μ-opioid receptor (μ-OR)-evoked respiratory depression. Here, we have tested whether such rescuing by serotonin agonists also applies to the cardiovascular system. In working heart–brainstem preparations in situ , we have recorded phrenic nerve activity, thoracic sympathetic chain activity (SCA), vascular resistance and heart rate (HR) and in conscious rats, diaphragmatic electromyogram, arterial blood pressure (BP) and HR via radio-telemetry. In addition, the distribution of 5-HT 4(a) R and 5-HT 1A R in ponto-medullary cardiorespiratory networks was identified using histochemistry. Systemic administration of the μ-OR agonist fentanyl in situ decreased HR, vascular resistance, SCA and phrenic nerve activity. Subsequent application of the 5-HT 1A R agonist 8-OH-DPAT further enhanced bradycardia, but partially compensated the decrease in vascular resistance, sympathetic activity and restored breathing. By contrast, the 5-HT 4(a) R agonist RS67333 further decreased vascular resistance, HR and sympathetic activity, but partially rescued breathing. In conscious rats, administration of remifentanyl caused severe respiratory depression, a decrease in mean BP accompanied by pronounced bradyarrhythmia. 8-OH-DPAT restored breathing and prevented the bradyarrhythmia; however, BP and HR remained below baseline. In contrast, RS67333 further suppressed cardiovascular functions in vivo and only partially recovered breathing in some cases. The better recovery of μ-OR cardiorespiratory disturbance by 5-HT 1A R than 5-HT 4(a) R is supported by the finding that 5-HT 1A R was more densely expressed in key brainstem nuclei for cardiorespiratory control compared with 5-HT 4(a) R. We conclude that during treatment of severe pain, 5-HT 1A R agonists may provide a useful tool to counteract opioid-mediated cardiorespiratory disturbances.
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Dissertations / Theses on the topic "Serotonin, control of breathing"

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Thomas, Dr Mike. "Dysfunctional breathing and asthma : can breathing exercises improve asthma control?" Thesis, University of Aberdeen, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531907.

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The hypothesis underlying this thesis was that abnormal, dysfunctional breathing may occur commonly in people with asthma, and when identified and treated using a breathing training programme supervised by a physiotherapist, will result in improved asthma control.  The thesis is based around four original research papers published in peer-reviewed journals.  These papers present epidemiological surveys quantifying the extent of symptoms attributable to dysfunctional breathing in adults with asthma in comparison with the non-asthmatic adult population, and randomised controlled trials investigating the effectiveness of a breathing training programme in improving asthma control. Initially, a review of the existing evidence of co-morbidity between asthma and dysfunctional breathing is presented, together with that of effectiveness of breathing training interventions.  In subsequent chapters, two epidemiological surveys are presented, showing that symptoms consistent with dysfunctional breathing were more common in the asthmatic than the non-asthmatic adult population.  Data from a pilot and a subsequent full randomised controlled trial are then presented.  These show that breathing training was associated with improved patient-reported outcomes in comparison with a control intervention of asthma education (chosen to control for the non-specific effects of professional contact and interest on a symptomatic patient). The thesis shows that in a clinical trial situation, many people with asthma can benefit from breathing training.
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Pearson, S. B. "Studies on the control of breathing." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235877.

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Brust, Rachael Danielle. "A specialized serotonergic neuron subtype transduces chemosensory signals and regulates breathing." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11401.

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Serotonergic neurons modulate a wide range of behaviors and functions, from mood and aggression to vital autonomic processes like heart rate, respiratory dynamics, and body temperature. We hypothesize that this broad scope reflects the collective actions of many functionally and molecularly distinct subtypes of serotonergic neurons, each with specialized roles in different neural processes. Supporting this idea are examples of heterogeneity among serotonergic neurons with respect to developmental origin, biophysical properties, and molecular expression; yet deciphering the functional and behavioral relevance of these differences has been challenging. In order to better understand serotonergic system organization, we have developed and applied a set of mouse genetic tools to subdivide serotonergic neurons into groups based on molecular criteria, and then to query these subtypes for differences with respect to biophysical properties, hodology, gene expression, and whole animal function. We applied these tools in a stage-wise fashion, from neural system en masse, as reference, and then to specific serotonergic neuron subtypes. From this, we have established that serotonergic neurons play key roles in at least two life-sustaining reflexes - the respiratory chemoreflex (breathing modulation to keep tissue PCO2/pH within physiological limits) and body temperature regulation. We found that chemoreflex modulation, but not body temperature regulation, maps to a specific serotonergic neuron subtype - that subtype with a developmental history of Egr2 gene expression. Further, in brain slice preparations, we found that this subtype is chemosensitive, increasing firing rate in response to conditions of hypercapnic acidosis. Thus, in vivo, Egr2-serotonergic neurons likely transduce chemosensory information into action potential firing to increase respiratory drive and ultimately breathing. Further, we found that Egr2-serotonergic neurons project selectively to respiratory nuclei involved in PCO2/pH sensory signal transduction, but not primary respiratory motor nuclei. This indicates that the serotonergic system has distinct sensory and motor divisions - another unexpected finding. In summary, these results establish a previously unappreciated functional modularity and organization to the serotonergic system, and open up potential for tailored function-specific therapeutic strategies, for example here as relates to disorders of respiratory homeostasis or thermoregulation.
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Silva, D. D. N. de. "Central control of breathing in animals under anaesthesia." Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238393.

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Andrews, David C. "Breathing control and thermoregulation in the developing lamb." Thesis, Oxford Brookes University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359674.

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Russell, Matthew. "DIAPHRAGMATIC BREATHING AND ITS EFFECT ON INHIBITORY CONTROL." UKnowledge, 2014. http://uknowledge.uky.edu/psychology_etds/53.

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Evidence suggests that slow paced diaphragmatic breathing (DB) can significantly affect prefrontal cortex functions through increasing an individual’s physiological self-regulatory capacity. The current research demonstrates the effects of paced DB on inhibitory control, which is considered to be a reliable measure of behavioral self-regulation. Eighty healthy participants were randomly assigned to one of two conditions (20 males and females each). Participants were instructed on either DB at a pace of six-breaths per minute (BPM) or instructions on environmental awareness and asked to breathe at 12 BPM. Following training, all participants completed a computer-based task designed to examine inhibitory processes. Physiological recordings of heart rate (HR), BPM, and HRV were collected at baseline, during the breathing training, during the cued go/no-go task, and after the cued go/no-go task. The findings demonstrated that the DB condition had significantly lower BPM, HR, and higher HRV (p’s<0.05) during active training than the environmental awareness condition. Furthermore, the DB condition performed significantly better on the measure of inhibition than the environmental awareness condition (p<0.05). The use of DB as a reliable method to increase physiological self-regulatory capacity and improve behavioral self-regulation, measured as inhibitory control, should continue to be explored.
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Tin, Chung 1980. "Afferents integration and neural adaptive control of breathing." Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/67603.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 2011.
Cataloged from PDF version of thesis.
Includes bibliographical references.
The respiratory regulatory system is one of the most extensively studied homeostatic systems in the body. Despite its deceptively mundane physiological function, the mechanism underlying the robust control of the motor act of breathing in the face of constantly changing internal and external challenges throughout one's life is still poorly understood. Traditionally, control of breathing has been studied with a highly reductionist approach, with specific stimulus-response relationships being taken to reflect distinct feedback/feedforward control laws. It is assumed that the overall respiratory response could be described as the linear sum of all unitary stimulus-response relationships under a Sherringtonian framework. Such a divide-and-conquer approach has proven useful in predicting the independent effects of specific chemical and mechanical inputs. However, it has limited predictive power for the respiratory response in realistic disease states when multiple factors come into play. Instead, vast amounts of evidence have revealed the existence of complex interactions of various afferent-efferent signals in defining the overall respiratory response. This thesis aims to explore the nonlinear interaction of afferents in respiratory control. In a series of computational simulations, it was shown that the respiratory response in humans during muscular exercise under a variety of pulmonary gas exchange defects is consistent with an optimal interaction of mechanical and chemical afferents. This provides a new understanding on the impacts of pulmonary gas exchange on the adaptive control of the exercise respiratory response. Furthermore, from a series of in-vivo neurophysiology experiments in rats, it was discovered that certain respiratory neurons in the dorsolateral pons in the rat brainstem integrate central and peripheral chemoreceptor afferent signals in a hypoadditive manner. Such nonlinear interaction evidences classical (Pavlovian) conditioning of chemoreceptor inputs that modulate the respiratory rhythm and motor output. These findings demonstrate a powerful gain modulation function for control of breathing by the lower brain. The computational and experimental studies in this thesis reveal a form of associative learning important for adaptive control of respiratory regulation, at both behavioral and neuronal levels. Our results shed new light for future experimental and theoretical elucidation of the mechanism of respiratory control from an integrative modeling perspective.
by Chung Tin.
Ph.D.
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Fiorentini, Lisa. "Nonlinear Adaptive Controller Design For Air-breathing Hypersonic Vehicles." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1274986563.

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Sigthorsson, David O. "Control-Oriented Modeling and Output Feedback Control of Hypersonic Air-Breathing Vehicles." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1228230786.

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Calder, Nicole Andrea. "Development of chemical control of breathing in the newborn." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243416.

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Books on the topic "Serotonin, control of breathing"

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Thomas, Schubert, and Karl Markovics. Atmen: Breathing. New York, NY: Kino Lorber, 2013.

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Chowdhuri, Susmita, M. Safwan Badr, and James A. Rowley. Control of Breathing during Sleep. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003000631.

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J, Whipp Brian, Physiological Society (Great Britain), and Teaching Symposium on "the Control of Breathing in Man" (1983 : St. George's Hospital Medical School), eds. The Control of breathing in man. Philadelphia, PA: University of Pennsylvania Press, 1987.

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Great Britain. Fire and Emergency Planning Directorate. Breathing apparatus: Command and control procedures. London: HMFSI/Stationery Office, 1997.

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Honda, Yoshiyuki, Yoshimi Miyamoto, Kimio Konno, and John G. Widdicombe, eds. Control of Breathing and Its Modeling Perspective. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4757-9847-0.

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Karczewski, W. A., P. Grieb, Joanna Kulesza, and G. Bonsignore, eds. Control of Breathing During Sleep and Anesthesia. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-9850-0.

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Poon, Chi-Sang, and Homayoun Kazemi, eds. Frontiers in Modeling and Control of Breathing. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1375-9.

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1926-, Honda Yoshiyuki, and Oxford Conference on Control of Breathing and its Modelling Perspective (5th : 1991 : Fuji-shi, Japan), eds. Control of breathing and its modeling perspective. New York: Plenum Press, 1992.

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International Symposium on Control of Breathing during Sleep and Anesthesia (1987 Warsaw, Poland). Control of breathing during sleep and anesthesia. New York: Plenum Press, 1988.

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Honda, Yoshiyuki. Control of Breathing and Its Modeling Perspective. Boston, MA: Springer US, 1992.

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Book chapters on the topic "Serotonin, control of breathing"

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Arita, Hideho, and Masahiro Sakamoto. "Role of Serotonin in Airway Patency: Physiological and Morphological Evidence for Serotoninergic Inputs to Laryngeal Inspiratory Motoneurons." In Control of Breathing and Its Modeling Perspective, 213–20. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4757-9847-0_37.

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Marazziti, D., G. Perugi, and G. B. Cassano. "Serotonin Control on Anxiety." In Serotonin, 543–48. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1912-9_71.

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Fozard, J. R., A. K. Mir, and A. G. Ramage. "5-HT1A Receptors and Cardiovascular Control." In Serotonin, 146–51. London: Palgrave Macmillan UK, 1989. http://dx.doi.org/10.1007/978-1-349-10114-6_19.

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Janssens, W. J., and J. M. Van Nueten. "Amplifying Effect of Serotonin in the Control of Vascular Tone." In Serotonin, 69–76. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1912-9_10.

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Teppema, Luc J., and Remco R. Berendsen. "Control of Breathing." In High Altitude, 37–55. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8772-2_3.

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Hornbien, Thomas F. "Control of Breathing." In Anesthesia and the Lung, 41–46. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0899-4_5.

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Moya, Esteban A., Tatum S. Simonson, Frank L. Powell, Robert L. Owens, and Atul Malhotra. "Control of Breathing." In Cardiopulmonary Monitoring, 205–18. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-73387-2_15.

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Bailey, Roy. "Stress control breathing." In MasterStress, 134–36. London: Routledge, 2021. http://dx.doi.org/10.4324/9781315169323-33.

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Wauquier, A., C. Dugovic, and P. A. J. Janssen. "Changing Views on the Role of Serotonergic Mechanisms in the Control of the Sleep-Wakefulness Cycle." In Serotonin, 187–91. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1912-9_24.

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Patz, David. "Breathing at Altitude." In Control of Breathing during Sleep, 168–81. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003000631-16.

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Conference papers on the topic "Serotonin, control of breathing"

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Borge, Christine Raheim, Ulrich Mack, Martha Lein, Anne Marit Mengshoel, Ernst Omenaas, Torbjørn Moum, and Astrid Wahl. "Fewer disease problems changes breathing pattern by breathing control exercises in COPD." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3739.

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Verbeuren, T. J., M. J. Van Diest, and A. G. Herman. "CONTRACTIONS TO PLATELETS IN AORTAS OF CONTROL AND CHOLESTEROL-FED RABBITS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643799.

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Atherosclerotic aortas obtained from cholesterol-fed rabbits show a decreased responsiveness to noradrenaline, an increased responsiveness to low concentrations of serotoninand an unaltered responsiveness to prostaglandins. In vitro contractions induced by aggregating platelets are largely due to serotonin liberated during the aggregation. The present study was designed to compare the contractile responses to aggregating platelets inaortas obtained from control and cholesterol-fed rabbits.Male New Zealand rabbits were fed either a control or a 0.3% cholesterol diet during 16 weeks. Macroscopic and microscopic examination of the luminal surface of the aortas obtained from these animals revealed a substantial amount of fatty streaks in the tissuesobtained from the cholesterol-fed rabbits. Segments of the aortic arch of the rabbits were then mounted in organ chambers for isometric tension recording.In both the control and the atherosclerotic aortas increasing concentrations of platelets evoked contractions; the contractions obtained with the lower concentrations of platelets were significantly greater in the atherosclerotic tissues. The maximal responses and the ED50-values were comparable in both groups of blood vessels. No significant differences were observed when platelets obtained from control or hypercholesterolemic rabbits were compared. In the control and the atherosclerotic aortas the thromboxane receptorantagonist BM13505 at 2 x 10-5M did not significantly affect the contractionsto platelets obtained from either control or cholesterol-fed rabbits. The serotonin receptor antagonist ketanserin at 5 x 10-8M nearly abolished the responses to platelets in bothgroups of aortas.These experiments illustrate that (1) thecontractions induced by rabbit platelets in control and atherosclerotic aortas are mediated by serotonin and (2) the responses to platelets, as those to serotonin, are augmented in the atherosclerotic preparations.
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TOWNEND, L. "Base pressure control for air-breathing launchers." In 26th Joint Propulsion Conference. Reston, Virigina: American Institute of Aeronautics and Astronautics, 1990. http://dx.doi.org/10.2514/6.1990-1936.

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Giannakopoulou, Charoula Eleni, Adamantia Sotiriou, Maria Dettoraki, Michael Yang, Fotis Perlikos, Dimitrios Toumpanakis, Georgios Prezerakos, et al. "Interleukin-10 affects the control of breathing." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2530.

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Giannakopoulou, Charoula Eleni, Maria Dettoraki, Adamantia Sotiriou, Charis Roussos, and Theodoros Vassilakopoulos. "Interleukin 10 Affects The Control Of Breathing." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4195.

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Van Buren, Mark A., and Kenneth D. Mease. "Minimum-Fuel Ascent to Orbit using Air-Breathing Propulsion." In 1989 American Control Conference. IEEE, 1989. http://dx.doi.org/10.23919/acc.1989.4790605.

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Tanaka, Mashiro. "Application of depth sensor for breathing rate counting." In 2015 10th Asian Control Conference (ASCC). IEEE, 2015. http://dx.doi.org/10.1109/ascc.2015.7244556.

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Veidal, Sandra, Asger Sverrild, Vibeke Backer, and Celeste Porsbjerg. "The role of dysfunctional breathing in asthma control." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa4480.

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PHILLIPS, STEPHEN, and DUANE MATTERN. "Feedback linearization for control of air breathing engines." In 27th Joint Propulsion Conference. Reston, Virigina: American Institute of Aeronautics and Astronautics, 1991. http://dx.doi.org/10.2514/6.1991-2000.

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Moriya, Rika, Mitsuko Kanamaru, Naoki Ookuma, Akira Yoshikawa, Kenji F. Tanaka, Satoshi Hokari, Yasuyoshi Ohshima, and Masahiko Izumizaki. "Optogenetic silencing of selected serotonin neurons in the control of CO2-induced arousal." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2299.

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Reports on the topic "Serotonin, control of breathing"

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Mustapha, Faremi. Serotonin, Etonogestrel and breathing activity in murine Congenital Central Hypoventilation Syndrome. ResearchHub Technologies, Inc., April 2022. http://dx.doi.org/10.55277/researchhub.4id705aq.

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Mustapha, Faremi. Serotonin, Etonogestrel and breathing activity in murine Congenital Central Hypoventilation Syndrome. ResearchHub Technologies, Inc., April 2022. http://dx.doi.org/10.55277/researchhub.4id705aq.

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Tan, Choon S., Kenneth Breuer, Thomas Corke, Jin-Woo Bae, and Robert Bayt. MEMS-Based Control for Air-Breathing Propulsion. Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada387696.

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Groves, Kevin P., Andrea Serrani, Stephen Yurkovich, Michael A. Bolender, and David B. Doman. Anti-Windup Control for an Air-Breathing Hypersonic Vehicle Model. Fort Belvoir, VA: Defense Technical Information Center, December 2005. http://dx.doi.org/10.21236/ada444973.

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Nakamura, Yusuke, Dong-Won Jung, and Norimasa Iida. Closed-Loop Combustion Control of a HCCI Engine with Re-Breathing EGR System. Warrendale, PA: SAE International, October 2013. http://dx.doi.org/10.4271/2013-32-9069.

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El Halawani, Mohamed, and Israel Rozenboim. Environmental factors affecting the decline in reproductive efficiency of turkey hens: Mediation by vasoactive intestinal peptide. United States Department of Agriculture, January 2007. http://dx.doi.org/10.32747/2007.7696508.bard.

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Reproductive failure associated with heat stress is a well known phenomenon in avian species. Increased prolactin (PRL) levels in response to heat stress have been suggested as a mechanism involved in this reproductive malfunction. To test this hypothesis, laying female turkeys were subjected to 40°C for 12 h during the photo-phase daily or maintained at 24–26°C. Birds in each group received oral treatment with parachlorophenyalanine (PCPA; 50 mg/kg BW/day for 3 days), an inhibitor of serotonin (5-HT) biosynthesis; or immunized against vasoactive intestinal peptide (VIP). Both treatments are known to reduce circulating PRL levels. Non treated birds were included as controls. In the control group, high ambient temperature terminated egg laying, induced ovarian regression, reduced plasma luteinizing hormone (LH) and ovarian steroids (progesterone, testosterone, estradiol) levels, and increased plasma PRL levels and the incidence of incubation behavior. Pretreatment with PCPA reduced (P< 0.05) heat stress-induced decline in egg production, increase in PRL levels, and expression of incubation behavior. Plasma LH and ovarian steroid levels of heat stressed birds were restored to that of controls by PCPA treatment. As in PCPA-treated birds, VIP immunoneutralization of heat-stressed turkeys reduced (P< 0.05) circulating PRL levels and prevented the expression of incubation behavior. But it did not restore the decline in LH, ovarian steroids, and egg production (P> 0.05). The present findings indicate that the detrimental effect of high temperature on reproductive performance may not be related to the elevated PRL levels in heat-stressed birds but to mechanism(s) that involve 5-HT neurotransmission and the induction of hyperthermia.
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