Journal articles: '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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Corcoran, Andrea E., George B. Richerson, and Michael B. Harris. "Functional link between the hypocretin and serotonin systems in the neural control of breathing and central chemosensitivity." Journal of Neurophysiology 114, no. 1 (July 2015): 381–89. http://dx.doi.org/10.1152/jn.00870.2013.

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Serotonin (5-HT)-synthesizing neurons of the medullary raphe are putative central chemoreceptors, proposed to be one of potentially multiple brain stem chemosensitive cell types and loci interacting to produce the respiratory chemoreflex. Hypocretin-synthesizing neurons of the lateral hypothalamus are important contributors to arousal state, thermoregulation, and feeding behavior and are also reportedly involved in the hypercapnic ventilatory response. Recently, a functional interaction was found between the hypocretin system and 5-HT neurons of the dorsal raphe. The validity and potential significance of hypocretin modulation of medullary raphe 5-HT neurons, however, is unknown. As such, the purpose of this study was to explore functional interactions between the hypocretin system and 5-HT system of the medullary raphe on baseline respiratory output and central chemosensitivity. To explore such interactions, we used the neonatal in vitro medullary slice preparation derived from wild-type (WT) mice (normal 5-HT function) and a knockout strain lacking all central 5-HT neurons ( Lmx1b f/f/p mice). We examined effects of acidosis, hypocretin-1, a hypocretin receptor antagonist (SB-408124), and the effect of the antagonist on the response to acidosis. We confirmed the critical role of 5-HT neurons in central chemosensitivity given that the increased hypoglossal burst frequency with acidosis, characteristic of WT mice, was absent in preparations derived from Lmx1b f/f/p mice. We also found that hypocretin facilitated baseline neural ventilatory output in part through 5-HT neurons. Although the impact of hypocretin on 5-HT neuronal sensitivity to acidosis is still unclear, hypocretins did appear to mediate the burst duration response to acidosis via serotonergic mechanisms.

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Hawkins, Virginia E., Joanna M. Hawryluk, Ana C. Takakura, Anastasios V. Tzingounis, Thiago S. Moreira, and Daniel K. Mulkey. "HCN channels contribute to serotonergic modulation of ventral surface chemosensitive neurons and respiratory activity." Journal of Neurophysiology 113, no. 4 (February 15, 2015): 1195–205. http://dx.doi.org/10.1152/jn.00487.2014.

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Chemosensitive neurons in the retrotrapezoid nucleus (RTN) provide a CO2/H+-dependent drive to breathe and function as an integration center for the respiratory network, including serotonergic raphe neurons. We recently showed that serotonergic modulation of RTN chemoreceptors involved inhibition of KCNQ channels and activation of an unknown inward current. Hyperpolarization-activated cyclic-nucleotide-gated (HCN) channels are the molecular correlate of the hyperpolarization-activated inward current ( Ih) and have a high propensity for modulation by serotonin. To investigate whether HCN channels contribute to basal activity and serotonergic modulation of RTN chemoreceptors, we characterize resting activity and the effects of serotonin on RTN chemoreceptors in vitro and on respiratory activity of anesthetized rats in the presence or absence of blockers of KCNQ (XE991) and/or HCN (ZD7288, Cs+) channels. We found in vivo that bilateral RTN injections of ZD7288 increased respiratory activity and in vitro HCN channel blockade increased activity of RTN chemoreceptors under control conditions, but this was blunted by KCNQ channel inhibition. Furthermore, in vivo unilateral RTN injection of XE991 plus ZD7288 eliminated the serotonin response, and in vitro serotonin sensitivity was eliminated by application of XE991 and ZD7288 or SQ22536 (adenylate cyclase blocker). Serotonin-mediated activation of RTN chemoreceptors was blocked by a 5-HT7-receptor blocker and mimicked by a 5-HT7-receptor agonist. In addition, serotonin caused a depolarizing shift in the voltage-dependent activation of Ih. These results suggest that HCN channels contribute to resting chemoreceptor activity and that serotonin activates RTN chemoreceptors and breathing in part by a 5-HT7 receptor-dependent mechanism and downstream activation of Ih.

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Manzke, Till, Marcus Niebert, Uwe R. Koch, Alex Caley, Steffen Vogelgesang, Swen Hülsmann, Evgeni Ponimaskin, et al. "Serotonin receptor 1A–modulated phosphorylation of glycine receptor α3 controls breathing in mice." Journal of Clinical Investigation 120, no. 11 (November 1, 2010): 4118–28. http://dx.doi.org/10.1172/jci43029.

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Muere, Clarissa, Suzanne Neumueller, Justin Miller, Samantha Olesiak, Matthew R. Hodges, Lawrence Pan, and Hubert V. Forster. "Atropine microdialysis within or near the pre-Bötzinger Complex increases breathing frequency more during wakefulness than during NREM sleep." Journal of Applied Physiology 114, no. 5 (March 1, 2013): 694–704. http://dx.doi.org/10.1152/japplphysiol.00634.2012.

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Normal activity of neurons within the medullary ventral respiratory column (VRC) in or near the pre-Bötzinger Complex (preBötC) is dependent on the balance of inhibitory and excitatory neuromodulators acting at their respective receptors. The role of cholinergic neuromodulation during awake and sleep states is unknown. Accordingly, our objective herein was to test the hypotheses that attenuation of cholinergic modulation of VRC/preBötC neurons in vivo with atropine would: 1) decrease breathing frequency more while awake than during non-rapid-eye-movement (NREM) sleep and 2) increase other excitatory neuromodulators. To test these hypotheses, we unilaterally dialyzed mock cerebrospinal fluid (mCSF) or 50 mM atropine in mCSF in or near the preBötC region of adult goats during the awake ( n = 9) and NREM sleep ( n = 7) states. Breathing was monitored, and effluent dialysate was collected for analysis of multiple neurochemicals. Compared with dialysis of mCSF alone, atropine increased ( P < 0.05) breathing frequency while awake during the day [+10 breaths (br)/min] and at night (+9 br/min) and, to a lesser extent, during NREM sleep (+5 br/min). Atropine increased ( P < 0.05) effluent concentrations of serotonin (5-HT), substance P (SP), and glycine during the day and at night. When atropine was dialyzed in one preBötC and mCSF in the contralateral preBötC, 5-HT and SP increased only at the site of atropine dialysis. We conclude: 1) attenuation of a single neuromodulator results in local changes in other neuromodulators that affect ventilatory control, 2) effects of perturbations of cholinergic neuromodulation on breathing are state-dependent, and 3) interpretation of perturbations in vivo requires consideration of direct and indirect effects.

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Penatti, Eliana M., Alexis E. Barina, Sharat Raju, Aihua Li, Hannah C. Kinney, Kathryn G. Commons, and Eugene E. Nattie. "Maternal dietary tryptophan deficiency alters cardiorespiratory control in rat pups." Journal of Applied Physiology 110, no. 2 (February 2011): 318–28. http://dx.doi.org/10.1152/japplphysiol.00788.2010.

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Malnutrition during pregnancy adversely affects postnatal forebrain development; its effect upon brain stem development is less certain. To evaluate the role of tryptophan [critical for serotonin (5-HT) synthesis] on brain stem 5-HT and the development of cardiorespiratory function, we fed dams a diet ∼45% deficient in tryptophan during gestation and early postnatal life and studied cardiorespiratory variables in the developing pups. Deficient pups were of normal weight at postnatal day (P)5 but weighed less than control pups at P15 and P25 ( P < 0.001) and had lower body temperatures at P15 ( P < 0.001) and P25 ( P < 0.05; females only). Oxygen consumption (V̇o2) was unaffected. At P15, deficient pups had an altered breathing pattern and slower heart rates. At P25, they had significantly lower ventilation (V̇e) and V̇e-to-V̇o2 ratios in both air and 7% CO2. The ventilatory response to CO2 (% increase in V̇e/V̇o2) was significantly increased at P5 (males) and reduced at P15 and P25 (males and females). Deficient pups had 41–56% less medullary 5-HT ( P < 0.01) compared with control pups, without a difference in 5-HT neuronal number. These data indicate important interactions between nutrition, brain stem physiology, and age that are potentially relevant to understanding 5-HT deficiency in the sudden infant death syndrome.

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Kuo, Fu-Shan, Bárbara Falquetto, Dawei Chen, Luiz M. Oliveira, Ana C. Takakura, and Daniel K. Mulkey. "In vitro characterization of noradrenergic modulation of chemosensitive neurons in the retrotrapezoid nucleus." Journal of Neurophysiology 116, no. 3 (September 1, 2016): 1024–35. http://dx.doi.org/10.1152/jn.00022.2016.

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Chemosensitive neurons in the retrotrapezoid nucleus (RTN) regulate breathing in response to CO2/H+ changes and serve as an integration center for other autonomic centers, including brain stem noradrenergic neurons. Norepinephrine (NE) contributes to respiratory control and chemoreception, and, since disruption of NE signaling may contribute to several breathing disorders, we sought to characterize effects of NE on RTN chemoreception. All neurons included in this study responded similarly to CO2/H+ but showed differential sensitivity to NE; we found that NE activated (79%), inhibited (7%), or had no effect on activity (14%) of RTN chemoreceptors. The excitatory effect of NE on RTN chemoreceptors was dose dependent, retained in the presence of neurotransmitter receptor blockers, and could be mimicked and blocked by pharmacological manipulation of α1-adrenergic receptors (ARs). In addition, NE-activation was blunted by XE991 (KCNQ channel blocker), and partially occluded the firing response to serotonin, suggesting involvement of KCNQ channels. However, in whole cell voltage clamp, activation of α1-ARs decreased outward current and conductance by what appears to be a mixed effect on multiple channels. The inhibitory effect of NE on RTN chemoreceptors was blunted by an α2-AR antagonist. A third group of RTN chemoreceptors was insensitive to NE. We also found that chemosensitive RTN astrocytes do not respond to NE with a change in voltage or by releasing ATP to enhance activity of chemosensitive neurons. These results indicate NE modulates subsets of RTN chemoreceptors by mechanisms involving α1- and α2-ARs.

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Langer, Thomas M., Suzanne E. Neumueller, Emma Crumley, Nicholas J. Burgraff, Sawan Talwar, Matthew R. Hodges, Lawrence Pan, and Hubert V. Forster. "Ventilation and neurochemical changes during µ-opioid receptor activation or blockade of excitatory receptors in the hypoglossal motor nucleus of goats." Journal of Applied Physiology 123, no. 6 (December 1, 2017): 1532–44. http://dx.doi.org/10.1152/japplphysiol.00592.2017.

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Neuromodulator interdependence posits that changes in one or more neuromodulators are compensated by changes in other modulators to maintain stability in the respiratory control network. Herein, we studied compensatory neuromodulation in the hypoglossal motor nucleus (HMN) after chronic implantation of microtubules unilaterally ( n = 5) or bilaterally ( n = 5) into the HMN. After recovery, receptor agonists or antagonists in mock cerebrospinal fluid (mCSF) were dialyzed during the awake and non-rapid eye movement (NREM) sleep states. During day studies, dialysis of the µ-opioid inhibitory receptor agonist [d-Ala2, N-MePhe4, Gly-ol]enkephalin (DAMGO; 100 µM) decreased pulmonary ventilation (V̇i), breathing frequency ( f), and genioglossus (GG) muscle activity but did not alter neuromodulators measured in the effluent mCSF. However, neither unilateral dialysis of a broad spectrum muscarinic receptor antagonist (atropine; 50 mM) nor unilateral or bilateral dialysis of a mixture of excitatory receptor antagonists altered V̇i or GG activity, but all of these did increase HMN serotonin (5-HT) levels. Finally, during night studies, DAMGO and excitatory receptor antagonist decreased ventilatory variables during NREM sleep but not during wakefulness. These findings contrast with previous dialysis studies in the ventral respiratory column (VRC) where unilateral DAMGO or atropine dialysis had no effects on breathing and bilateral DAMGO or unilateral atropine increased V̇i and f and decreased GABA or increased 5-HT, respectively. Thus we conclude that the mechanisms of compensatory neuromodulation are less robust in the HMN than in the VRC under physiological conditions in adult goats, possibly because of site differences in the underlying mechanisms governing neuromodulator release and consequently neuronal activity, and/or responsiveness of receptors to compensatory neuromodulators. NEW & NOTEWORTHY Activation of inhibitory µ-opioid receptors in the hypoglossal motor nucleus decreased ventilation under physiological conditions and did not affect neurochemicals in effluent dialyzed mock cerebral spinal fluid. These findings contrast with studies in the ventral respiratory column where unilateral [d-Ala2, N-MePhe4, Gly-ol]enkephalin (DAMGO) had no effects on ventilation and bilateral DAMGO or unilateral atropine increased ventilation and decreased GABA or increased serotonin, respectively. Our data support the hypothesis that mechanisms that govern local compensatory neuromodulation within the brain stem are site specific under physiological conditions.

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Magnusson, Jennifer, and Kevin J. Cummings. "Plasticity in breathing and arterial blood pressure following acute intermittent hypercapnic hypoxia in infant rat pups with a partial loss of 5-HT neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 309, no. 10 (November 15, 2015): R1273—R1284. http://dx.doi.org/10.1152/ajpregu.00241.2015.

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The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied in the neonatal period. We hypothesized that a partial loss of 5-HT neurons would reduce arterial blood pressure (BP) at rest, increase the fall in BP during hypoxia, and reduce the long-term facilitation of breathing (vLTF) and BP following AIH. We exposed 2-wk-old, 5,7-dihydroxytryptamine-treated and controls to AIH (10% O2; n = 13 control, 14 treated), acute intermittent hypercapnia (5% CO2; n = 12 and 11), or acute intermittent hypercapnic hypoxia (AIHH; 10% O2, 5% CO2; n = 15 and 17). We gave five 5-min challenges of AIH and acute intermittent hypercapnia, and twenty ∼20-s challenges of AIHH to mimic sleep apnea. Systolic BP (sBP), diastolic BP, mean arterial pressure, heart rate (HR), ventilation (V̇e), and metabolic rate (V̇o2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% loss of 5-HT neurons from the medullary raphe. Compared with controls, pups deficient in 5-HT neurons had reduced resting sBP (∼6 mmHg), mean arterial pressure (∼5 mmHg), and HR (56 beats/min), and experienced a reduced drop in BP during hypoxia. AIHH induced vLTF in both groups, reflected in increased V̇e and V̇e/V̇o2, and decreased arterial Pco2. The sBP of pups deficient in 5-HT neurons, but not controls, was increased 1 h following AIHH. Our data suggest that a relatively small loss of 5-HT neurons compromises resting BP and HR, but has no influence on ventilatory plasticity induced by AIHH. AIHH may be useful for reversing cardiorespiratory defects related to partial 5-HT system dysfunction.

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Lovell, Natasha, Sabrina Bajwah, Matthew Maddocks, Andrew Wilcock, and Irene J. Higginson. "Use of mirtazapine in patients with chronic breathlessness: A case series." Palliative Medicine 32, no. 9 (July 20, 2018): 1518–21. http://dx.doi.org/10.1177/0269216318787450.

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Background: Breathlessness remains a common and distressing symptom in people with advanced disease with few effective treatment options. Repurposing of existing medicines has been effective in other areas of palliative care, for example, antidepressants to treat pain, and offers an opportunity to deliver improved symptom control in a timely manner. Previous case series have shown reduced breathlessness following the use of sertraline (a selective serotonin reuptake inhibitor) in people with chronic obstructive pulmonary disease. Cases: Six cases where mirtazapine, a noradrenergic and specific serotonergic antidepressant, was used to treat chronic breathlessness in advanced lung disease. Case management: All cases received mirtazapine at a starting dose of 15 mg, prescribed under the care of their primary care physician. Cases had been receiving mirtazapine for a variable time period (2 weeks to 5 months) at the time of the interviews. Case outcome: All cases reported less breathlessness and being able to do more. They described feeling more in control of their breathing, and being able to recover more quickly from episodes of breathlessness. Some cases also reported beneficial effects on anxiety, panic, appetite and sleep. No adverse effects were reported. Discussion: Patients with chronic breathlessness in this case series reported benefits during mirtazapine treatment. To determine the effectiveness of mirtazapine in alleviating breathlessness and improving quality of life in chronic lung disease, blinded randomised trials are warranted.

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Gruenthal, Eric, Nancy Foldvary-Schaefer, Lu Wang, Alex Milinovich, Carl Saab, Julia Bucklan, and Reena Mehra. "0639 Polysomnographic Biomarkers of Sleep Disruption and Sleep Disordered Breathing in Migraine: a Large Matched Case Control Clinical Registry-Based Study." Sleep 45, Supplement_1 (May 25, 2022): A281. http://dx.doi.org/10.1093/sleep/zsac079.636.

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Abstract Introduction Sleep disruption and sleep architectural changes in relation to migraine are not well characterized. Disruption in sleep may serve as a risk for migraine or result from migraine. We leveraged a large clinical cohort to examine the hypothesis that those with migraine have greater degrees of sleep architectural alterations and sleep disordered breathing (SDB). Methods This was a polysomnogram-based retrospective case (migraine) control (non-migraine) study of patients aged >18 matched 1:3 on age, sex, race, body mass index (BMI), and year of polysomnogram. Two domains were considered: 1)Sleep architecture (arousal index:AI, (primary predictor), total sleep time (TST), percentage of sleep stage time) and 2)SDB (apnea hypopnea index (AHI:primary predictor), mean oxygen saturation) were considered. Comparisons were performed by two-sample t-test or Wilcoxon rank sum test for continuous variables, and chi-square test or Fisher’s exact test for categorical variables. Results 4,783 migraine cases (47.5 ±13.3 years, 76.4% Caucasian, body mass index:BMI 33.7 ±8.6kg/m2) were matched to 14,287 controls. In migraine patients vs those without, TST was lower (359.0[307.0, 421.0] minutes vs 363.0[306.0, 432.5] minutes,p=0.01), percentage of N2 was higher (67.8%[59.6, 75.6] vs 67.0%[58.4, 74.8],p<0.001), percentage of REM was lower (16.7% [10.0, 22.0] vs 17.0% [11.1, 22.2],p=0.012), AHI was lower (7.4 [2.6, 17.0] vs 9.5 [3.7, 22.1],p<0.001), AI was lower (19.6 [12.8, 30.9] vs 22.6 [14.7, 34.9],p<0.001), and mean oxygen saturation was higher (93.7%±2.4 vs 93.3±2.6,p<0.001). Conclusion In this largest study of its kind, we identify novel associations of migraine in relation to curtailed sleep and sleep architectural alterations, i.e. increase in N2 and reduced REM sleep and lower AI compared to contemporaneously matched controls. Directionality of these relationships requires further elucidation given the cross-sectional nature of this study. Interestingly, we observed lower degree of sleep apnea and hypoxia burden in patients with migraine. As Calcitonin Gene-Related Peptide (CGRP), a neuropeptide increased during and between migraine attacks in migraine patients, and serotonin are implicated in arousals due to apnea-related increases in CO2, there is biologic plausibility for migraines patients to exhibit potential protection from SDB. Further investigation is needed to confirm these findings. Support (If Any)

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Varney, Abrea A., and Evelyn H. Schlenker. "Thyroid status affects 5-HT2A receptor modulation of breathing before, during, and following exposure of hamsters to acute intermittent hypoxia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 5 (November 2007): R2070—R2080. http://dx.doi.org/10.1152/ajpregu.00495.2007.

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The BIO 14.6 hamster (dystrophic), animal model of limb girdle muscular dystrophy, exhibits low plasma triiodothyronine levels, muscle weakness, and decreased breathing. After exposure to acute intermittent bouts of hypoxia, dystrophic hamsters depress ventilation relative to baseline resulting in ventilatory long-term depression (LTD). Control hamsters may increase ventilation relative to baseline resulting in ventilatory long-term facilitation (LTF). Serotonin (5-HT) receptors, especially the 5-HT2A subtype, are involved in the development of LTF. The purpose of this study was to evaluate the role of 5-HT2A receptors in ventilatory and metabolic responses before, during, and following intermittent hypoxia in eleven euthyroid, nine dystrophic, and eleven propylthiouracil (PTU)-induced hypothyroid male hamsters. Animals received subcutaneous injections of vehicle or 0.5 mg/kg MDL (5-HT2A receptor antagonist). Plethysmography was used to evaluate ventilatory responses of the three groups to air, five bouts of 5 min of 10% oxygen, each interspersed with 5 min of air, followed by 60 min of exposure to air. CO2 production was measured using the flow-through method. Vehicle-treated dystrophic and PTU-treated hamsters exhibited LTD. MDL decreased body temperature in all groups. After MDL treatment, the euthyroid group exhibited LTD. MDL treatment in the dystrophic, but not in the PTU-treated hamsters, maintained tidal volume, but did not reverse LTD. CO2 production was increased in the euthyroid group with MDL treatment. Thus, 5-HT2A receptors affect body temperature, ventilation, and metabolism in hamsters. The differential responses noted in this study may be in part dependent on thyroid hormone status.

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Arita, H., and M. Ochiishi. "Opposing effects of 5-hydroxytryptamine on two types of medullary inspiratory neurons with distinct firing patterns." Journal of Neurophysiology 66, no. 1 (July 1, 1991): 285–92. http://dx.doi.org/10.1152/jn.1991.66.1.285.

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1. Activity of inspiratory neurons was recorded extracellularly from the caudal portion of the nucleus ambiguous (0–3.5 mm rostral to the obex) in decerebrated, spontaneously breathing cats. Using a micropressure ejection method, we tested the responsiveness of the inspiratory neurons to direct applications of serotonin (5-HT) and noradrenaline (NA) in comparison with applications of glutamate and control artificial cerebrospinal fluid (ACSF) by means of a multibarreled micropipette. 2. We made detailed examinations of 52 inspiratory neurons that were excited by glutamate but did not react to control ACSF. Those inspiratory neurons were further classified into two subgroups based on the differences in firing patterns: inspiratory neurons with an augmenting firing pattern ["augmenting I units" (22/52)] and inspiratory neurons with a decrementing firing pattern [“decrementing I units” (30/52)]. 3. Although application of NA produced predominantly inhibitory effects on both the decrementing (22/30) and augmenting I units (20/22), application of 5-HT resulted in distinct or opposing effects on these two types of inspiratory neurons: the decrementing I units (25/30, 83%) were excited by 5-HT, whereas the augmenting I units (17/22, 77%) were inhibited by 5-HT. 4. The excitation of the decrementing I units with 5-HT was characterized by a long onset-latency of response and a prolonged recovery process. The increase in firing rate occurred not only during the inspiratory active phase but also during the expiratory phase.(ABSTRACT TRUNCATED AT 250 WORDS)

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Langer, Thomas M., Suzanne E. Neumueller, Emma Crumley, Nicholas J. Burgraff, Sawan Talwar, Matthew R. Hodges, Lawrence Pan, and Hubert V. Forster. "State-dependent and -independent effects of dialyzing excitatory neuromodulator receptor antagonists into the ventral respiratory column." Journal of Applied Physiology 122, no. 2 (February 1, 2017): 327–38. http://dx.doi.org/10.1152/japplphysiol.00619.2016.

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Unilateral dialysis of the broad-spectrum muscarinic receptor antagonist atropine (50 mM) into the ventral respiratory column [(VRC) including the pre-Bötzinger complex region] of awake goats increased pulmonary ventilation (V̇i) and breathing frequency (f), conceivably due to local compensatory increases in serotonin (5-HT) and substance P (SP) measured in effluent mock cerebral spinal fluid (mCSF). In contrast, unilateral dialysis of a triple cocktail of antagonists to muscarinic (atropine; 5 mM), neurokinin-1, and 5-HT receptors does not alter V̇i or f, but increases local SP. Herein, we tested hypotheses that 1) local compensatory 5-HT and SP responses to 50 mM atropine dialyzed into the VRC of goats will not differ between anesthetized and awake states; and 2) bilateral dialysis of the triple cocktail of antagonists into the VRC of awake goats will not alter V̇i or f, but will increase local excitatory neuromodulators. Through microtubules implanted into the VRC of goats, probes were inserted to dialyze mCSF alone (time control), 50 mM atropine, or the triple cocktail of antagonists. We found 1) equivalent increases in local 5-HT and SP with 50 mM atropine dialysis during wakefulness compared with isoflurane anesthesia, but V̇i and f only increased while awake; and 2) dialyses of the triple cocktail of antagonists increased V̇i, f, 5-HT, and SP (<0.05) during both day and night studies. We conclude that the mechanisms governing local neuromodulator levels are state independent, and that bilateral excitatory receptor blockade elicits an increase in breathing, presumably due to a local, (over)compensatory neuromodulator response. NEW & NOTEWORTHY The two major findings are as follows: 1) during unilateral dialysis of 50 mM atropine into the ventral respiratory column to block excitatory muscarinic receptor activity, a compensatory increase in other neuromodulators was state independent, but the ventilatory response appears to be state dependent; and 2) the hypothesis that absence of decreased V̇i and f during unilateral dialysis of excitatory receptor antagonists was due to compensation by the contralateral VRC was not supported by findings herein.

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MacFarlane, P. M., S. Vinit, and G. S. Mitchell. "Enhancement of phrenic long-term facilitation following repetitive acute intermittent hypoxia is blocked by the glycolytic inhibitor 2-deoxyglucose." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 314, no. 1 (January 1, 2018): R135—R144. http://dx.doi.org/10.1152/ajpregu.00306.2017.

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Moderate acute intermittent hypoxia (mAIH) elicits a form of respiratory motor plasticity known as phrenic long-term facilitation (pLTF). Preconditioning with modest protocols of chronic intermittent hypoxia enhances pLTF, demonstrating pLTF metaplasticity. Since “low-dose” protocols of repetitive acute intermittent hypoxia (rAIH) show promise as a therapeutic modality to restore respiratory (and nonrespiratory) motor function in clinical disorders with compromised breathing, we tested 1) whether preconditioning with a mild rAIH protocol enhances pLTF and hypoglossal (XII) LTF and 2) whether the enhancement is regulated by glycolytic flux. In anesthetized, paralyzed, and ventilated adult male Lewis rats, mAIH (three 5-min episodes of 10% O2) elicited pLTF (pLTF at 60 min post-mAIH: 49 ± 5% baseline). rAIH preconditioning (ten 5-min episodes of 11% O2/day with 5-min normoxic intervals, 3 times per week, for 4 wk) significantly enhanced pLTF (100 ± 16% baseline). XII LTF was unaffected by rAIH. When glycolytic flux was inhibited by 2-deoxy-d-glucose (2-DG) administered via drinking water (~80 mg·kg−1·day−1), pLTF returned to normal levels (58 ± 8% baseline); 2-DG had no effect on pLTF in normoxia-pretreated rats (59 ± 7% baseline). In ventral cervical (C4/5) spinal homogenates, rAIH increased inducible nitric oxide synthase mRNA vs. normoxic controls, an effect blocked by 2-DG. However, there were no detectable effects of rAIH or 2-DG on several molecules associated with phrenic motor plasticity, including serotonin 2A, serotonin 7, brain-derived neurotrophic factor, tropomyosin receptor kinase B, or VEGF mRNA. We conclude that modest, but prolonged, rAIH elicits pLTF metaplasticity and that a drug known to inhibit glycolytic flux (2-DG) blocks pLTF enhancement.

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Overstreet, David H., and Veljko Djuric. "Links between multiple chemical sensitivity and asthma in a rat model of cholinergic hypersensitivity: a brief review." Toxicology and Industrial Health 15, no. 5 (June 1999): 517–21. http://dx.doi.org/10.1177/074823379901500505.

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Individuals with multiple chemical sensitivity (MCS) also commonly report symptoms of asthma, but, as far as we have been able to determine, no one has yet suggested that an abnormal cholinergic system may provide the link between asthma and MCS. The present brief review provides evidence for such a link by summarizing recent findings in a genetic animal model of cholinergic hyperresponsiveness. The Flinders Sensitive Line (FSL) rats were developed by selective breeding for increased responses to an anticholinesterase agent similar to commonly used organophosphate pesticides. Relative to their control line, the Flinders Resistant Line (FRL) rats, the FSL rats are more sensitive to drugs that stimulate acetylcholine receptors, alcohol, diazepam, and drugs that have a selective effect on dopamine or serotonin receptors. These findings raise the possibility that the FSL rats may resemble individuals with MCS. Hyperresponsiveness of the airways is a hallmark of asthma. The procedure known as whole-body plethysmography, where breathing can be monitored in freely moving animals, was employed to study the FSL and FRL rats. The FSL rats exhibited a greater index of bronchoconstriction than the FRL rats in response to both a cholinergic agonist and an allergen challenge. Thus, the FSL rats are more sensitive both to a variety of drugs unrelated to the cholinergic system and to cholinergic- and allergen-induced bronchoconstriction. An abnormal cholinergic system may therefore contribute to both MCS and asthma.

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Richter, Diethelm W., Till Manzke, Bernd Wilken, and Evgeni Ponimaskin. "Serotonin receptors: guardians of stable breathing." Trends in Molecular Medicine 9, no. 12 (December 2003): 542–48. http://dx.doi.org/10.1016/j.molmed.2003.10.010.

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Sevoz, C., J. C. Callera, B. H. Machado, M. Hamon, and R. Laguzzi. "Role of serotonin3 receptors in the nucleus tractus solitarii on the carotid chemoreflex." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 3 (March 1, 1997): H1250—H1259. http://dx.doi.org/10.1152/ajpheart.1997.272.3.h1250.

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The effects of serotonin3 (5-HT3)-receptor stimulation in the nucleus tractus solitarii (NTS) on the cardiovagal, sympathetic, and respiratory responses to activation of carotid body chemoreceptors were investigated in anesthetized rats. The chemoreflex responses were triggered by an intravenous administration of KCN (40 microg/kg) in spontaneously breathing urethan-chloralose-anesthetized rats or by an intracarotid administration of saline saturated with 100% CO2 in pancuronium bromide-paralyzed and artificially ventilated urethan-anesthetized rats. Microinjections of 5-HT (2.5-5 nmol) or the 5-HT3 agonist 1-(m-chlorophenyl)-biguanide (CPBG, 300-1,200 pmol) into the commissural NTS blocked in a dose-dependent manner the atropine-sensitive chemoreflex bradycardia elicited by KCN. However, neither 5-HT nor CPBG affected the KCN-induced increase in respiratory volume and the CO2-induced increases in blood pressure and lumbar sympathetic nerve discharge. The inhibitory effect of 5-HT or CPBG on KCN-induced bradycardia was blocked by prior intra-NTS microinjection of a 5-HT3 antagonist, such as zacopride (100 pmol) or ondansetron (100 pmol), or the A-type gamma-aminobutyric acid (GABA(A)) antagonist bicuculline (10 pmol). In contrast, local microinjections of antagonists acting at 5-HT1 and 5-HT2 receptors, such as methysergide (100 pmol) and ketanserin (10 pmol), respectively, did not prevent the actions of 5-HT or CPBG. These data show that the stimulation of 5-HT3 receptors in the NTS exerted an inhibitory influence, probably through the activation of a local GABAergic system, on the cardiovagal component of the chemoreflex. Because similar effects of 5-HT3-receptor stimulation in the NTS were previously found on the baroreflex and Bezold-Jarisch reflex responses, it can be inferred that NTS 5-HT3 receptors play a key modulatory role in the reflex control of the heart rate.

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Nasim, Sobia, Faraz Jabbar, Asfar Afridi, and Brendan D. Kelly. "Serotonin toxicity." Irish Journal of Psychological Medicine 28, no. 2 (June 2011): i—iv. http://dx.doi.org/10.1017/s0790966700011599.

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Serotonin toxicity is a potentially life-threatening condition associated with a range of psychotropic medications, co-administration of specific combinations of agents and overdose of certain drugs. It is associated with a wide diversity of clinical signs and symptoms, including cognitive, autonomic and somatic effects, as well as serious complications, including possible death. Diagnosis is often challenging and requires a high index of suspicion. Differential diagnosis includes syndromes such as neuroleptic malignant syndrome. Management depends on the causal agent and urgency of clinical presentation. Treatment may involve discontinuing the causal agent and providing supportive measures, or emergency intervention to preserve vital functions (airway, breathing, circulation), amongst other measures. Further research is needed to clarify the incidence of serotonin toxicity, issues related to differential diagnosis, optimal management of the condition, and treatment of mood problems following serotonin toxicity.

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29

Jones, J. G. "Control of breathing." Current Opinion in Anaesthesiology 1, no. 4 (November 1988): 488–93. http://dx.doi.org/10.1097/00001503-198801040-00008.

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Jones, J. G. "Control of breathing." Current Opinion in Anaesthesiology 1, no. 4 (November 1988): 488–93. http://dx.doi.org/10.1097/00001503-198811000-00008.

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31

Goodman, N. W., and C. Dodds. "Control of breathing." Current Opinion in Anaesthesiology 2, no. 6 (December 1989): 782–88. http://dx.doi.org/10.1097/00001503-198912000-00018.

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32

Jansen, A. H., and V. Chernick. "Fetal breathing and development of control of breathing." Journal of Applied Physiology 70, no. 4 (April 1, 1991): 1431–46. http://dx.doi.org/10.1152/jappl.1991.70.4.1431.

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Technical advances during the last several decades have greatly facilitated research into fetal physiology and behavior, specifically fetal breathing (FB). Breathing movements have been demonstrated in the fetuses of every mammalian species investigated and appear to be part of normal fetal development. In this review we focus on the methods of measuring FB and on some of the problems associated with these measurements and their interpretation. We also review fetal behavior, the role of the peripheral and central chemoreceptors in spontaneous FB, the fetal respiratory response to hypercapnia and hypoxia, and the transition to continuous breathing at birth. It is clear that in many ways the control of breathing movements in utero differs from that after birth. In particular, inhibitory influences are much more prominent before than after birth. Possibly this is due to the unique fetal situation, in which conservation of energy may be more important than any advantage breathing activity imparts to the fetus.

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33

Zhang, Weirong, and Paul W. Davenport. "Neural Control of Breathing." Perspectives on Voice and Voice Disorders 15, no. 1 (March 2005): 20–24. http://dx.doi.org/10.1044/vvd15.1.20.

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34

Orem, J., and RH Trotter. "Behavioral Control in Breathing." Physiology 9, no. 5 (October 1, 1994): 228–32. http://dx.doi.org/10.1152/physiologyonline.1994.9.5.228.

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Cats trained to stop inspiration do so by inactivating inspiratory cells of the automatic brain stem control system. The cells causing this inactivation are not those that stop inspiration during normal breathing;rather, they may be peculiar cells with both respiratory and nonrespiratory properties.

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Dayan, Peter, and Quentin J. M. Huys. "Serotonin in Affective Control." Annual Review of Neuroscience 32, no. 1 (June 2009): 95–126. http://dx.doi.org/10.1146/annurev.neuro.051508.135607.

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Muere, Clarissa, Suzanne Neumueller, Samantha Olesiak, Justin Miller, Matthew R. Hodges, Lawrence Pan, and Hubert V. Forster. "Blockade of neurokinin-1 receptors in the ventral respiratory column does not affect breathing but alters neurochemical release." Journal of Applied Physiology 118, no. 6 (March 15, 2015): 732–41. http://dx.doi.org/10.1152/japplphysiol.00884.2014.

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Substance P (SP) and its receptor, neurokinin-1 (NK1R), have been shown to be excitatory modulators of respiratory frequency and to stabilize breathing regularity. Studies in anesthetized mice suggest that tonic activation of NK1Rs is particularly important when other excitatory inputs to the pre-Bötzinger complex in the ventral respiratory column (VRC) are attenuated. Consistent with these findings, muscarinic receptor blockade in the VRC of intact goats elicits an increase in breathing frequency associated with increases in SP and serotonin concentrations, suggesting an involvement of these substances in neuromodulator compensation. To gain insight on the contribution to breathing of endogenous SP and NK1R activation, and how NK1R modulates the release of other neurochemicals, we individually dialyzed antagonists to NK1R (133, 267, 500 μM Spantide; 3 mM RP67580) throughout the VRC of awake and sleeping goats. We found that NK1R blockade with either Spantide at any dose or RP67580 had no effect on breathing or regularity. Both antagonists significantly ( P < 0.001) increased SP, while RP67580 also increased serotonin and glycine and decreased thyrotropin-releasing hormone concentrations in the dialysate. Taken together, these data support the concept of neuromodulator interdependence, and we believe that the loss of excitatory input from NK1Rs was locally compensated by changes in other neurochemicals.

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YOSHIDA, Takayoshi, and Yoshiyuki FUKUBA. "Control of Breathing during Exercise." Annals of physiological anthropology 11, no. 5 (1992): 479–93. http://dx.doi.org/10.2114/ahs1983.11.479.

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Ward, Susan A. "Control of Breathing During Exercise." Colloquium Series on Integrated Systems Physiology: From Molecule to Function 6, no. 3 (July 31, 2014): 1–93. http://dx.doi.org/10.4199/c00108ed1v01y201406isp052.

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Teppema, Luc J., and Santhosh Baby. "Anesthetics and control of breathing." Respiratory Physiology & Neurobiology 177, no. 2 (July 2011): 80–92. http://dx.doi.org/10.1016/j.resp.2011.04.006.

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Grossman, E., A. Grossman, MH Schein, R. Zimlichman, and B. Gavish. "Breathing-control lowers blood pressure." Journal of Human Hypertension 15, no. 4 (April 2001): 263–69. http://dx.doi.org/10.1038/sj.jhh.1001147.

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Nogu�s, Mart�n A., Aquiles J. Roncoroni, and Eduardo Benarroch. "Breathing control in neurological diseases." Clinical Autonomic Research 12, no. 6 (December 1, 2002): 440–49. http://dx.doi.org/10.1007/s10286-002-0067-1.

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Yang, Liang, Gang Song, Yinghui Ning, and Chi-Sang Poon. "A latent serotonin-1A receptor-gated spinal afferent pathway inhibiting breathing." Brain Structure and Function 221, no. 8 (December 12, 2015): 4159–68. http://dx.doi.org/10.1007/s00429-015-1155-z.

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Gaultier, C. "Genetics, control of breathing, and sleep-disordered breathing: a review." Sleep Medicine 2, no. 4 (July 2001): 281–95. http://dx.doi.org/10.1016/s1389-9457(01)00098-3.

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Komnenov, Dragana, Julia Z. Solarewicz, Fareeza Afzal, Kwaku D. Nantwi, Donald M. Kuhn, and Jason H. Mateika. "Intermittent hypoxia promotes recovery of respiratory motor function in spinal cord-injured mice depleted of serotonin in the central nervous system." Journal of Applied Physiology 121, no. 2 (August 1, 2016): 545–57. http://dx.doi.org/10.1152/japplphysiol.00448.2016.

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We examined the effect of repeated daily exposure to intermittent hypoxia (IH) on the recovery of respiratory and limb motor function in mice genetically depleted of central nervous system serotonin. Electroencephalography, diaphragm activity, ventilation, core body temperature, and limb mobility were measured in spontaneously breathing wild-type (Tph2+/+) and tryptophan hydroxylase 2 knockout (Tph2−/−) mice. Following a C2 hemisection, the mice were exposed daily to IH (i.e., twelve 4-min episodes of 10% oxygen interspersed with 4-min normoxic periods followed by a 90-min end-recovery period) or normoxia (i.e., sham protocol, 21% oxygen) for 10 consecutive days. Diaphragm activity recovered to prehemisection levels in the Tph2+/+ and Tph2−/− mice following exposure to IH but not normoxia [Tph2+/+ 1.3 ± 0.2 (SE) vs. 0.3 ± 0.2; Tph2−/− 1.06 ± 0.1 vs. 0.3 ± 0.1, standardized to prehemisection values, P < 0.01]. Likewise, recovery of tidal volume and breathing frequency was evident, although breathing frequency values did not return to prehemisection levels within the time frame of the protocol. Partial recovery of limb motor function was also evident 2 wk after spinal cord hemisection. However, recovery was not dependent on IH or the presence of serotonin in the central nervous system. We conclude that IH promotes recovery of respiratory function but not basic motor tasks. Moreover, we conclude that spontaneous or treatment-induced recovery of respiratory and motor limb function is not dependent on serotonin in the central nervous system in a mouse model of spinal cord injury.

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Hickner, Stephen, Najaah Hussain, Mariana Angoa-Perez, Dina M. Francescutti, Donald M. Kuhn, and Jason H. Mateika. "Ventilatory long-term facilitation is evident after initial and repeated exposure to intermittent hypoxia in mice genetically depleted of brain serotonin." Journal of Applied Physiology 116, no. 3 (February 1, 2014): 240–50. http://dx.doi.org/10.1152/japplphysiol.01197.2013.

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Our study was designed to determine if central nervous system (CNS) serotonin is required for the induction of ventilatory long-term facilitation (LTF) in intact, spontaneously breathing mice. Nineteen tryptophan hydroxylase 2-deficient (Tph2−/−) mice, devoid of serotonin in the CNS, and their wild-type counterparts (Tph2+/+) were exposed to intermittent hypoxia each day for 10 consecutive days. The ventilatory response to intermittent hypoxia was greater in the Tph2+/+ compared with the Tph2−/− mice (1.10 ± 0.10 vs. 0.77 ± 0.01 ml min−1·percent−1 oxygen; P ≤ 0.04). Ventilatory LTF, caused by increases in breathing frequency, was evident in Tph2+/+ and Tph2−/− mice following exposure to intermittent hypoxia each day; however, the magnitude of the response was greater in the Tph2+/+ compared with the Tph2−/− mice (1.11 ± 0.02 vs. 1.05 ± 0.01 normalized to baseline on each day; P ≤ 0.01). The magnitude of ventilatory LTF increased significantly from the initial to the finals days of the protocol in the Tph2−/− (1.06 ± 0.02 vs. 1.11 ± 0.03 normalized to baseline on the initial days; P ≤ 0.004) but not in the Tph2+/+ mice. This enhanced response was mediated by increases in tidal volume. Body temperature and metabolic rate did not account for differences in the magnitude of ventilatory LTF observed between groups after acute and repeated daily exposure to intermittent hypoxia. We conclude that ventilatory LTF, after acute exposure to intermittent hypoxia, is mediated by increases in breathing frequency and occurs in the absence of serotonin, although the magnitude of the response is diminished. This weakened response is enhanced following repeated daily exposure to intermittent hypoxia, via increases in tidal volume, to a similar magnitude evident in Tph2+/+ mice. Thus the magnitude of ventilatory LTF following repeated daily exposure to intermittent hypoxia is not dependent on the presence of CNS serotonin.

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Denny, Margaret, and Anne Smith. "Respiratory Control in Stuttering Speakers." Journal of Speech, Language, and Hearing Research 43, no. 4 (August 2000): 1024–37. http://dx.doi.org/10.1044/jslhr.4304.1024.

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This study tested the hypothesis that, in stuttering speakers, relations between the neural control systems for speech and life support, or metabolic breathing, may differ from relations previously observed in normally fluent subjects. Bilaterally coherent high-frequency oscillations in inspiratory-related EMGs, measured as maximum coherence in the frequency band of 60–110 Hz (MC-HFO), were used as indicators of participation by the brainstem controller for metabolic breathing in 10 normally fluent and 10 stuttering speakers. In all controls and most stuttering subjects, MC-HFO for speech was higher than or comparable to MC-HFO for deep breathing. For 4 stuttering subjects, higher MC-HFO was observed for speech than for deep breathing. Comparison of deep breathing to a speechlike breathing task yielded similar results. No relationship between MC-HFO during speech and severity of disfluency was observed. We conclude that in some stuttering speakers, the relations between respiratory controllers are atypical, but that high participation by the HFO-producing circuitry in the brainstem during speech is not sufficient to disrupt fluency.

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PEARSON, HEATHER J. "Paraphilias, Impulse Control, and Serotonin." Journal of Clinical Psychopharmacology 10, no. 3 (June 1990): 233. http://dx.doi.org/10.1097/00004714-199006000-00027.

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Milsom, William K. "Control of arrhythmic breathing in aerial breathers." Canadian Journal of Zoology 66, no. 1 (January 1, 1988): 99–108. http://dx.doi.org/10.1139/z88-014.

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Arrhythmic breathing patterns of two basic types occur among the air-breathing vertebrates. These patterns, which appear to be dependent more on inputs from peripheral receptor groups than on a central generator, allow significant fluctuations in the partial pressures of O2 and CO2 in lungs, blood, and tissues with accompanying fluctuations of pH in body fluids. The major components of each pattern are the size and timing of each breath, the length of each episode of breathing, and the length of the pause between episodes of breathing. While each of these components appears to be under separate control, the relative roles of the various receptor groups in the control of each remain unclear. Similarities between data collected from reptiles and hibernating mammals suggest that the arrhythmic breathing patterns seen under physiological conditions in all air-breathing vertebrates may be manifestations of a common control system. The conversion from continuous to arrhythmic breathing seen in mammals entering hibernation further suggests that both continuous and arrhythmic breathing are manifestations of a common control system. The two distinct arrhythmic breathing patterns appear to arise from differences in the supramedullary integration of vagal input in different species. It is suggested that under conditions of reduced metabolic demand, these arrhythmic breathing patterns may represent an adaptive strategy which, in part, serves to reduce the energetic cost of ventilation.

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Menuet, Clément, Nazim Kourdougli, Gérard Hilaire, and Nicolas Voituron. "Differences in serotoninergic metabolism possibly contribute to differences in breathing phenotype of FVB/N and C57BL/6J mice." Journal of Applied Physiology 110, no. 6 (June 2011): 1572–81. http://dx.doi.org/10.1152/japplphysiol.00117.2011.

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Mouse readiness for gene manipulation allowed the production of mutants with breathing defects reminiscent of breathing syndromes. As C57BL/6J and FVB/N inbred strains were often used as background strains for producing mutants, we compared their breathing pattern from birth onwards. At birth, in vivo and in vitro approaches revealed robust respiratory rhythm in FVB/N, but not C57BL/6J, neonates. With aging, rhythm robustness difference persisted, and interstrain differences in tidal volume, minute ventilation, breathing regulations, and blood-gas parameters were observed. As serotonin affected maturation and function of the medullary respiratory network, we examined the serotoninergic metabolism in the medulla of C57BL/6J and FVB/N neonates and aged mice. Interstrain differences in serotoninergic metabolism were observed at both ages. We conclude that differences in serotoninergic metabolism possibly contribute to differences in breathing phenotype of FVB/N and C57BL/6J mice.

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Zaccone, Giacomo, Eugenia Rita Lauriano, Gioele Capillo, and Michał Kuciel. "Air- breathing in fish: Air- breathing organs and control of respiration." Acta Histochemica 120, no. 7 (October 2018): 630–41. http://dx.doi.org/10.1016/j.acthis.2018.08.009.

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

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