Journal articles on the topic 'Chemoreceptors'
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1
Lazovic, Biljana, Mirjana Zlatkovic-Svenda, Tijana Durmic, Zoran Stajic, Vesna Djuric, and Vladimir Zugic. "The regulation role of carotid body peripheral chemoreceptors in physiological and pathophysiological conditions." Medical review 69, no. 11-12 (2016): 385–90. http://dx.doi.org/10.2298/mpns1612385l.
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Introduction. The major oxygen sensors in the human body are peripheral chemoreceptors, also known as interoreceptors-as connected with internal organs, located in the aortic arch and in the body of the common carotid artery. Chemoreceptor function under physiological conditions. Stimulation of peripheral chemoreceptors during enviromental hypoxia causes a reflex-mediated increased ventilation, followed by the increase of the muscle sympatic activity, aiming to maintain tissue oxygen homeostatis, as well as glucosae homeostatis. Besides that, peripheral chemoreceptors interact with central chemoreceptors, responsible for carbon dioxide changes, and they are able to modulate each other. Chemoreceptor function in pathophysiological conditions. Investigations of respiratory function in many pathological processes, such as hypertension, obstructive sleep apnea, congestive heart failure and many other diseases that are presented with enhanced peripheral chemosensitivity and impaired functional sympatholysis ultimately determine the peripheral chemoreceptor role and significance of peripheral chemoreceptors in the process of those pathological conditions development. Considering this, the presumed influence of peripheral chemoreceptors is important in patients having the above mentioned pathology. Conclusion. The importance and the role of peripheral chemoreceptors in the course of the breathing control is still controversial, despite many scientific attempts to solve this problem. The main objective of this review is to give the latest data on the peripheral chemoreceptor role and to highlight the importance of peripheral chemoreceptors for maintaining of oxygen homeostasis in pateints with hypoxia caused by either physiological or pathological conditions.
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Lybarger, Suzanne R., and Janine R. Maddock. "Clustering of the Chemoreceptor Complex inEscherichia coli Is Independent of the Methyltransferase CheR and the Methylesterase CheB." Journal of Bacteriology 181, no. 17 (September 1, 1999): 5527–29. http://dx.doi.org/10.1128/jb.181.17.5527-5529.1999.
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ABSTRACT The Escherichia coli chemoreceptors and their associated cytoplasmic proteins, CheA and CheW, cluster predominantly at the cell poles. The nature of the clustering remains a mystery. Recent studies suggest that CheR binding to and/or methylation of the chemoreceptors may play a role in chemoreceptor complex aggregation. In this study, we examined the intracellular distribution of the chemoreceptors by immunoelectron microscopy in strains lacking either the methyltransferase CheR or the methylesterase CheB. The localization data revealed that, in vivo, aggregation of the chemoreceptor complex was independent of either CheR or CheB.
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Collins, Kieran D., Tessa M. Andermann, Jenny Draper, Lisa Sanders, Susan M. Williams, Cameron Araghi, and Karen M. Ottemann. "The Helicobacter pylori CZB Cytoplasmic Chemoreceptor TlpD Forms an Autonomous Polar Chemotaxis Signaling Complex That Mediates a Tactic Response to Oxidative Stress." Journal of Bacteriology 198, no. 11 (March 21, 2016): 1563–75. http://dx.doi.org/10.1128/jb.00071-16.
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ABSTRACTCytoplasmic chemoreceptors are widespread among prokaryotes but are far less understood than transmembrane chemoreceptors, despite being implicated in many processes. One such cytoplasmic chemoreceptor isHelicobacter pyloriTlpD, which is required for stomach colonization and drives a chemotaxis response to cellular energy levels. Neither the signals sensed by TlpD nor its molecular mechanisms of action are known. We report here that TlpD functions independently of the other chemoreceptors. When TlpD is the sole chemoreceptor, it is able to localize to the pole and recruits CheW, CheA, and at least two CheV proteins to this location. It loses the normal membrane association that appears to be driven by interactions with other chemoreceptors and with CheW, CheV1, and CheA. These results suggest that TlpD can form an autonomous signaling unit. We further determined that TlpD mediates a repellent chemotaxis response to conditions that promote oxidative stress, including being in the presence of iron, hydrogen peroxide, paraquat, and metronidazole. Last, we found that all testedH. pyloristrains express TlpD, whereas other chemoreceptors were present to various degrees. Our data suggest a model in which TlpD coordinates a signaling complex that responds to oxidative stress and may allowH. pylorito avoid areas of the stomach with high concentrations of reactive oxygen species.IMPORTANCEHelicobacter pylorisenses its environment with proteins called chemoreceptors. Chemoreceptors integrate this sensory information to affect flagellum-based motility in a process called chemotaxis. Chemotaxis is employed during infection and presumably aidsH. pyloriin encountering and colonizing preferred niches. A cytoplasmic chemoreceptor named TlpD is particularly important in this process, and we report here that this chemoreceptor is able to operate independently of other chemoreceptors to organize a chemotaxis signaling complex and mediate a repellent response to oxidative stress conditions.H. pyloriencounters and must cope with oxidative stress during infection due to oxygen and reactive oxygen species produced by host cells. TlpD's repellent response may allow the bacteria to escape niches experiencing inflammation and elevated reactive oxygen species (ROS) production.
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Prabhakar, Nanduri R., and Ying-Jie Peng. "Peripheral chemoreceptors in health and disease." Journal of Applied Physiology 96, no. 1 (January 2004): 359–66. http://dx.doi.org/10.1152/japplphysiol.00809.2003.
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Peripheral chemoreceptors (carotid and aortic bodies) detect changes in arterial blood oxygen and initiate reflexes that are important for maintaining homeostasis during hypoxemia. This mini-review summarizes the importance of peripheral chemoreceptor reflexes in various physiological and pathophysiological conditions. Carotid bodies are important for eliciting hypoxic ventilatory stimulation in humans and in experimental animals. In the absence of carotid bodies, compensatory upregulation of aortic bodies as well as other chemoreceptors contributes to the hypoxic ventilatory response. Peripheral chemoreceptors are critical for ventilatory acclimatization at high altitude. They also contribute in part to the exercise-induced hyperventilation, especially with submaximal and heavy exercise. During pregnancy, hypoxic ventilatory sensitivity increases, perhaps due to the actions of estrogen and progesterone on chemoreceptors. Augmented peripheral chemoreceptors have been implicated in early stages of recurrent apneas, congestive heart failure, and certain forms of hypertension. It is likely that chemoreceptors tend to maintain oxygen homeostasis and act as a defense mechanism to prevent the progression of the morbidity associated with these diseases. Experimental models of recurrent apneas, congestive heart failure, and hypertension offer excellent opportunities to unravel the cellular mechanisms associated with altered chemoreceptor function.
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García, Vanina, Jose-Antonio Reyes-Darias, David Martín-Mora, Bertrand Morel, Miguel A. Matilla, and Tino Krell. "Identification of a Chemoreceptor for C2and C3Carboxylic Acids." Applied and Environmental Microbiology 81, no. 16 (June 5, 2015): 5449–57. http://dx.doi.org/10.1128/aem.01529-15.
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ABSTRACTChemoreceptors are at the beginnings of chemosensory signaling cascades that mediate chemotaxis. Most bacterial chemoreceptors are functionally unannotated and are characterized by a diversity in the structure of their ligand binding domains (LBDs). The data available indicate that there are two major chemoreceptor families at the functional level, namely, those that respond to amino acids or to Krebs cycle intermediates. Since pseudomonads show chemotaxis to many different compounds and possess different types of chemoreceptors, they are model organisms to establish relationships between chemoreceptor structure and function. Here, we identify PP2861 (termed McpP) ofPseudomonas putidaKT2440 as a chemoreceptor with a novel ligand profile. We show that the recombinant McpP LBD recognizes acetate, pyruvate, propionate, andl-lactate, withKD(equilibrium dissociation constant) values ranging from 34 to 107 μM. Deletion of themcpPgene resulted in a dramatic reduction in chemotaxis toward these ligands, and complementation restored a native-like phenotype, indicating that McpP is the major chemoreceptor for these compounds. McpP has a CACHE-type LBD, and we present data indicating that CACHE-containing chemoreceptors of other species also mediate taxis to C2and C3carboxylic acids. In addition, the LBD of NbaY ofPseudomonas fluorescens, an McpP homologue mediating chemotaxis to 2-nitrobenzoate, bound neither nitrobenzoates nor the McpP ligands. This work provides further insight into receptor structure-function relationships and will be helpful to annotate chemoreceptors of other bacteria.
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Ortega, Davi R., Aaron D. Fleetwood, Tino Krell, Caroline S. Harwood, Grant J. Jensen, and Igor B. Zhulin. "Assigning chemoreceptors to chemosensory pathways in Pseudomonas aeruginosa." Proceedings of the National Academy of Sciences 114, no. 48 (November 13, 2017): 12809–14. http://dx.doi.org/10.1073/pnas.1708842114.
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In contrast to Escherichia coli, a model organism for chemotaxis that has 5 chemoreceptors and a single chemosensory pathway, Pseudomonas aeruginosa PAO1 has a much more complex chemosensory network, which consists of 26 chemoreceptors feeding into four chemosensory pathways. While several chemoreceptors were rigorously linked to specific pathways in a series of experimental studies, for most of them this information is not available. Thus, we addressed the problem computationally. Protein–protein interaction network prediction, coexpression data mining, and phylogenetic profiling all produced incomplete and uncertain assignments of chemoreceptors to pathways. However, comparative sequence analysis specifically targeting chemoreceptor regions involved in pathway interactions revealed conserved sequence patterns that enabled us to unambiguously link all 26 chemoreceptors to four pathways. Placing computational evidence in the context of experimental data allowed us to conclude that three chemosensory pathways in P. aeruginosa utilize one chemoreceptor per pathway, whereas the fourth pathway, which is the main system controlling chemotaxis, utilizes the other 23 chemoreceptors. Our results show that while only a very few amino acid positions in receptors, kinases, and adaptors determine their pathway specificity, assigning receptors to pathways computationally is possible. This requires substantial knowledge about interacting partners on a molecular level and focusing comparative sequence analysis on the pathway-specific regions. This general principle should be applicable to resolving many other receptor–pathway interactions.
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Gaudel, Fanny, Gaëlle Guiraudie-Capraz, and François Féron. "Limbic Expression of mRNA Coding for Chemoreceptors in Human Brain—Lessons from Brain Atlases." International Journal of Molecular Sciences 22, no. 13 (June 25, 2021): 6858. http://dx.doi.org/10.3390/ijms22136858.
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Animals strongly rely on chemical senses to uncover the outside world and adjust their behaviour. Chemical signals are perceived by facial sensitive chemosensors that can be clustered into three families, namely the gustatory (TASR), olfactory (OR, TAAR) and pheromonal (VNR, FPR) receptors. Over recent decades, chemoreceptors were identified in non-facial parts of the body, including the brain. In order to map chemoreceptors within the encephalon, we performed a study based on four brain atlases. The transcript expression of selected members of the three chemoreceptor families and their canonical partners was analysed in major areas of healthy and demented human brains. Genes encoding all studied chemoreceptors are transcribed in the central nervous system, particularly in the limbic system. RNA of their canonical transduction partners (G proteins, ion channels) are also observed in all studied brain areas, reinforcing the suggestion that cerebral chemoreceptors are functional. In addition, we noticed that: (i) bitterness-associated receptors display an enriched expression, (ii) the brain is equipped to sense trace amines and pheromonal cues and (iii) chemoreceptor RNA expression varies with age, but not dementia or brain trauma. Extensive studies are now required to further understand how the brain makes sense of endogenous chemicals.
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Smith, C. A., J. R. Rodman, B. J. A. Chenuel, K. S. Henderson, and J. A. Dempsey. "Response time and sensitivity of the ventilatory response to CO2 in unanesthetized intact dogs: central vs. peripheral chemoreceptors." Journal of Applied Physiology 100, no. 1 (January 2006): 13–19. http://dx.doi.org/10.1152/japplphysiol.00926.2005.
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We assessed the speed of the ventilatory response to square-wave changes in alveolar Pco2 and the relative gains of the steady-state ventilatory response to CO2 of the central chemoreceptors vs. the carotid body chemoreceptors in intact, unanesthetized dogs. We used extracorporeal perfusion of the reversibly isolated carotid sinus to maintain normal tonic activity of the carotid body chemoreceptor while preventing it from sensing systemic changes in CO2, thereby allowing us to determine the response of the central chemoreceptors alone. We found the following. 1) The ventilatory response of the central chemoreceptors alone is 11.2 (SD = 3.6) s slower than when carotid bodies are allowed to sense CO2 changes. 2) On average, the central chemoreceptors contribute ∼63% of the gain to steady-state increases in CO2. There was wide dog-to-dog variability in the relative contributions of central vs. carotid body chemoreceptors; the central exceeded the carotid body gain in four of six dogs, but in two dogs carotid body gain exceeded central CO2 gain. If humans respond similarly to dogs, we propose that the slower response of the central chemoreceptors vs. the carotid chemoreceptors prevents the central chemoreceptors from contributing significantly to ventilatory responses to rapid, transient changes in arterial Pco2 such as those after periods of hypoventilation or hyperventilation (“ventilatory undershoots or overshoots”) observed during sleep-disordered breathing. However, the greater average responsiveness of the central chemoreceptors to brain hypercapnia in the steady-state suggests that these receptors may contribute significantly to ventilatory overshoots once unstable/periodic breathing is fully established.
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Fortier, Emma M., Sophie Bouillet, Pascale Infossi, Amine Ali Chaouche, Leon Espinosa, Marie-Thérèse Giudici-Orticoni, Emilia M. F. Mauriello, and Chantal Iobbi-Nivol. "Defining Two Chemosensory Arrays in Shewanella oneidensis." Biomolecules 13, no. 1 (December 22, 2022): 21. http://dx.doi.org/10.3390/biom13010021.
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Shewanella oneidensis has 2 functional chemosensory systems named Che1 and Che3, and 27 chemoreceptors. Che3 is dedicated to chemotaxis while Che1 could be involved in RpoS post-translational regulation. In this study, we have shown that two chemoreceptors Aer2so and McpAso, genetically related to the Che1 system, form distinct core-signaling units and signal to Che1 and Che3, respectively. Moreover, we observed that Aer2so is a cytoplasmic dynamic chemoreceptor that, when in complex with CheA1 and CheW1, localizes at the two poles and the centre of the cells. Altogether, the results obtained indicate that Che1 and Che3 systems are interconnected by these two chemoreceptors allowing a global response for bacterial survival.
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Khursigara, Cezar M., Xiongwu Wu, and Sriram Subramaniam. "Chemoreceptors in Caulobacter crescentus: Trimers of Receptor Dimers in a Partially Ordered Hexagonally Packed Array." Journal of Bacteriology 190, no. 20 (August 8, 2008): 6805–10. http://dx.doi.org/10.1128/jb.00640-08.
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ABSTRACT Chemoreceptor arrays are macromolecular complexes that form extended assemblies primarily at the poles of bacterial cells and mediate chemotaxis signal transduction, ultimately controlling cellular motility. We have used cryo-electron tomography to determine the spatial distribution and molecular architecture of signaling molecules that comprise chemoreceptor arrays in wild-type Caulobacter crescentus cells. We demonstrate that chemoreceptors are organized as trimers of receptor dimers, forming partially ordered hexagonally packed arrays of signaling complexes in the cytoplasmic membrane. This novel organization at the threshold between order and disorder suggests how chemoreceptors and associated molecules are arranged in signaling assemblies to respond dynamically in the activation and adaptation steps of bacterial chemotaxis.
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Smatresk, N. J. "Chemoreceptor modulation of endogenous respiratory rhythms in vertebrates." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 259, no. 5 (November 1, 1990): R887—R897. http://dx.doi.org/10.1152/ajpregu.1990.259.5.r887.
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The relative contributions of O2- and CO2-sensitive chemoreceptor information to centrally generated respiratory patterns have changed dramatically during vertebrate evolution. Chemoafferent input from branchial O2 chemoreceptors modulates centrally generated respiratory patterns but is not critical for respiratory rhythmogenesis in fishes. In air-breathing fishes, branchial O2 chemoreceptors monitoring internal and external stimuli control the relative contributions of the gills and air-breathing organ to net ventilation, and chemoafferent input is necessary for initiating air breathing. In the transition from water to air breathing by amphibious vertebrates, rhythmic patterns of branchial ventilation are completely replaced by arrhythmic and intermittent patterns of air breathing, and there is progressive dependence on CO2 as a source of respiratory drive. Periodic initiation of air breathing in resting animals appears to depend on attaining a threshold level of afferent activity from O2- and CO2/pH-sensitive chemoreceptors, since hyperoxia and/or hypocapnia can abolish air breathing in all air-breathing vertebrates. Conversely, chemoreceptor stimulation in amphibians and reptiles converts intermittent to more continuous air breathing patterns, suggesting that adequate biasing input from chemoreceptors activates a central rhythm generator. Chemoafferent input in homeotherms serves as one of several sources of drive for rhythmic breathing and supplies feedback for blood gas homeostasis in the face of metabolic or environmental change.
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McCoy, K. W., D. M. Rotto, and M. P. Kaufman. "Inhibition of aortic chemoreceptor discharge by pressor response to muscular contraction." Journal of Applied Physiology 62, no. 6 (June 1, 1987): 2258–63. http://dx.doi.org/10.1152/jappl.1987.62.6.2258.
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We have examined the effect of static contraction of the hindlimb muscles on the discharge of aortic chemoreceptors in chloralose-anesthetized cats. The responses of the chemoreceptors to contraction were dependent on the arterial pressure response to this maneuver. When contraction reflexly evoked a pressor response of at least 20 mmHg, the discharge of 26 chemoreceptors was reduced from control levels by 53% (P less than 0.01). The contraction-induced inhibition of chemoreceptor discharge was prevented by phentolamine, an alpha-adrenergic antagonist that also attenuated the contraction-induced pressor response. In addition, the inhibition evoked by contraction was simulated by injection of phenylephrine and inflation of an aortic balloon, both of which evoked pressor responses. However, when contraction failed to significantly change arterial pressure, the discharge of 20 aortic chemoreceptors was not significantly changed from control levels. We conclude that the reflex pressor response to static contraction inhibits the discharge of aortic chemoreceptors. This inhibition of discharge needs to be considered when interpreting the effects of aortic barodenervation on the cardiovascular responses to exercise.
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Dempsey, Jerome A., and Curtis A. Smith. "Do Carotid Chemoreceptors Inhibit the Hyperventilatory Response to Heavy Exercise?" Canadian Journal of Applied Physiology 19, no. 3 (September 1, 1994): 350–59. http://dx.doi.org/10.1139/h94-028.
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In this paper two types of evidence are presented which question the commonly presumed role of carotid chemoreceptor stimulation as the primary mediator of the hyperventilatory response to heavy exercise. First, carotid-body denervation in ponies increases their hyperventilatory response to heavy exercise. Second, the awake dog and the goat at rest show an immediate and substantial depression of tidal volume and of ventilation when their isolated carotid chemoreceptors are made hypocapnic. Accordingly, it is proposed that during heavy exercise the carotid chemoreceptors are inhibitory to respiratory motor output and that the cause of the hyperventilatory response originates from extrachemoreceptor, locomotor-linked, feed-forward stimuli. Key words: hypocapnic inhibition, medullary chemoreceptors, locomotor-linked stimuli, feed-forward
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Smith, C. A., B. J. Chenuel, K. S. Henderson, and J. A. Dempsey. "The apneic threshold during non-REM sleep in dogs: sensitivity of carotid body vs. central chemoreceptors." Journal of Applied Physiology 103, no. 2 (August 2007): 578–86. http://dx.doi.org/10.1152/japplphysiol.00017.2007.
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The relative importance of peripheral vs. central chemoreceptors in causing apnea/unstable breathing during sleep is unresolved. This has never been tested in an unanesthetized preparation with intact carotid bodies. We studied three unanesthetized dogs during normal sleep in a preparation in which intact carotid body chemoreceptors could be reversibly isolated from the systemic circulation and perfused. Apneic thresholds and the CO2 reserve (end-tidal Pco2 eupneic − end-tidal Pco2 apneic threshold) were determined using a pressure support ventilation technique. Dogs were studied when both central and peripheral chemoreceptors sensed transient hypocapnia induced by the pressure support ventilation and again with carotid body isolation such that only the central chemoreceptors sensed the hypocapnia. We observed that the CO2 reserve was ≅4.5 Torr when the carotid chemoreceptors sensed the transient hypocapnia but more than doubled (>9 Torr) when only the central chemoreceptors sensed hypocapnia. Furthermore, the expiratory time prolongations observed when only central chemoreceptors were exposed to hypocapnia differed from those obtained when both the central and peripheral chemoreceptors sensed the hypocapnia in that they 1) were substantially shorter for a given reduction in end-tidal Pco2, 2) showed no stimulus: response relationship with increasing hypocapnia, and 3) often occurred at a time (>45 s) beyond the latency expected for the central chemoreceptors. These findings agree with those previously obtained using an identical pressure support ventilation protocol in carotid body-denervated sleeping dogs (Nakayama H, Smith CA, Rodman JR, Skatrud JB, Dempsey JA. J Appl Physiol 94: 155–164, 2003). We conclude that hypocapnia sensed at the carotid body chemoreceptor is required for the initiation of apnea following a transient ventilatory overshoot in non-rapid eye movement sleep.
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Huang, Zhiwei, Junnan Zou, Minliang Guo, Guoliang Zhang, Jun Gao, Hongliang Zhao, Feiyu Yan, Yuan Niu, and Guang-Long Wang. "An aerotaxis receptor influences invasion of Agrobacterium tumefaciens into its host." PeerJ 12 (February 5, 2024): e16898. http://dx.doi.org/10.7717/peerj.16898.
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Agrobacterium tumefaciens is a soil-borne pathogenic bacterium that causes crown gall disease in many plants. Chemotaxis offers A. tumefaciens the ability to find its host and establish infection. Being an aerobic bacterium, A. tumefaciens possesses one chemotaxis system with multiple potential chemoreceptors. Chemoreceptors play an important role in perceiving and responding to environmental signals. However, the studies of chemoreceptors in A. tumefaciens remain relatively restricted. Here, we characterized a cytoplasmic chemoreceptor of A. tumefaciens C58 that contains an N-terminal globin domain. The chemoreceptor was designated as Atu1027. The deletion of Atu1027 not only eliminated the aerotactic response of A. tumefaciens to atmospheric air but also resulted in a weakened chemotactic response to multiple carbon sources. Subsequent site-directed mutagenesis and phenotypic analysis showed that the conserved residue His100 in Atu1027 is essential for the globin domain’s function in both chemotaxis and aerotaxis. Furthermore, deleting Atu1027 impaired the biofilm formation and pathogenicity of A. tumefaciens. Collectively, our findings demonstrated that Atu1027 functions as an aerotaxis receptor that affects agrobacterial chemotaxis and the invasion of A. tumefaciens into its host.
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Zhang, W., and S. W. Mifflin. "Excitatory amino acid receptors within NTS mediate arterial chemoreceptor reflexes in rats." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 2 (August 1, 1993): H770—H773. http://dx.doi.org/10.1152/ajpheart.1993.265.2.h770.
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The nucleus tractus solitarius (NTS) is the primary site of termination of arterial baroreceptor and chemoreceptor afferent fibers. Excitatory amino acid (EAA) receptors within NTS have been shown to play an important role in the mediation of arterial baroreceptor reflexes; however, the importance of EAA receptors within NTS in the mediation of arterial chemoreceptor reflexes remains controversial. Therefore, in chloralose-urethan-anesthetized, mechanically ventilated, paralyzed rats, 4 nmol of the broad-spectrum EAA receptor antagonist kynurenic acid (Kyn) was injected into the NTS to observe the effects of EAA receptor blockade on the pressor responses evoked by either activation of ipsilateral carotid body chemoreceptors (by close arterial injection of CO2-saturated bicarbonate) or electrical stimulation of ipsilateral carotid sinus nerve (CSN). Under control conditions, activation of carotid body chemoreceptors and CSN stimulation evoked increases in arterial pressure of 27 +/- 2 (n = 24 sites) and 28 +/- 3% (n = 8), respectively. Kyn microinjection into NTS significantly reduced the pressor responses evoked by activation of carotid body chemoreceptors and electrical stimulation of the CSN for 20 and 25 min, respectively. Attenuation of pressor responses evoked by chemoreceptor activation were maximal at 20 min post-Kyn injection (13 +/- 2%), whereas CSN-evoked pressor responses were maximally attenuated at 15 min (6 +/- 4%). Microinjection into NTS of 4 nmol of xanthurenic acid, a structural analogue of Kyn with no EAA receptor antagonist properties, had no effect on chemoreceptor reflexes. We conclude that EAA receptors within NTS play an important role in the mediation of arterial chemoreceptor reflexes.
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Praud, J. P., E. Canet, I. Kianicka, C. Gaultier, and M. Bureau. "Vagal and chemoreceptor influences on abdominal muscle activity in awake lambs during hypoxia." Journal of Applied Physiology 74, no. 4 (April 1, 1993): 1689–96. http://dx.doi.org/10.1152/jappl.1993.74.4.1689.
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The ventilatory response to hypoxia is a complex phenomenon involving several control mechanisms. We designed this study to examine the dynamic control of abdominal muscle expiratory electromyogram (EMG) activity during room-air breathing and hypoxia and then to analyze the relative contribution of the chemoreceptors and vagal afferents. We studied 12 11- to 22-day-old awake nonsedated lambs, six intact and six vagotomized. To assess the dynamic influence of peripheral chemoreceptors on abdominal muscle expiratory activity, we performed transient testing of peripheral chemoreceptor function (pure O2 and N2 inhalation, KCN injection). To assess the influence of central chemoreceptor afferents, we compared results obtained during hypocapnic and isocapnic 15-min hypoxic runs (fractional concentration of inspired O2 0.08) in each lamb. We also compared results obtained in intact and vagotomized lambs so that the importance of vagal afferents could be assessed. We consistently observed abdominal muscle expiratory EMG activity in each lamb, whether intact or vagotomized, during baseline room air breathing; further recruitment was observed during hypoxia. We also consistently observed abdominal muscle expiratory recruitment during hypocapnic hypoxia in each lamb, although it was significantly less marked than during isocapnic hypoxia. Our transient testing of peripheral chemoreceptor function showed, furthermore, that peripheral chemoreceptor afferents dynamically modulate abdominal muscle expiratory activity. Thus, during hypoxia in 11- to 22-day-old awake nonsedated lambs, increased afferent information from peripheral chemoreceptors forcefully enhances abdominal muscle expiratory activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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Nuding, Sarah C., Lauren S. Segers, Roger Shannon, Russell O'Connor, Kendall F. Morris, and Bruce G. Lindsey. "Central and peripheral chemoreceptors evoke distinct responses in simultaneously recorded neurons of the raphé-pontomedullary respiratory network." Philosophical Transactions of the Royal Society B: Biological Sciences 364, no. 1529 (September 12, 2009): 2501–16. http://dx.doi.org/10.1098/rstb.2009.0075.
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The brainstem network for generating and modulating the respiratory motor pattern includes neurons of the medullary ventrolateral respiratory column (VRC), dorsolateral pons (PRG) and raphé nuclei. Midline raphé neurons are proposed to be elements of a distributed brainstem system of central chemoreceptors, as well as modulators of central chemoreceptors at other sites, including the retrotrapezoid nucleus. Stimulation of the raphé system or peripheral chemoreceptors can induce a long-term facilitation of phrenic nerve activity; central chemoreceptor stimulation does not. The network mechanisms through which each class of chemoreceptor differentially influences breathing are poorly understood. Microelectrode arrays were used to monitor sets of spike trains from 114 PRG, 198 VRC and 166 midline neurons in six decerebrate vagotomized cats; 356 were recorded during sequential stimulation of both receptor classes via brief CO 2 -saturated saline injections in vertebral (central) and carotid arteries (peripheral). Seventy neurons responded to both stimuli. More neurons were responsive only to peripheral challenges than those responsive only to central chemoreceptor stimulation (PRG, 20 : 4; VRC, 41 : 10; midline, 25 : 13). Of 16 474 pairs of neurons evaluated for short-time scale correlations, similar percentages of reference neurons in each brain region had correlation features indicative of a specific interaction with at least one target neuron: PRG (59.6%), VRC (51.0%) and raphé nuclei (45.8%). The results suggest a brainstem network architecture with connectivity that shapes the respiratory motor pattern via overlapping circuits that modulate central and peripheral chemoreceptor-mediated influences on breathing.
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Mifflin, S. W. "Arterial chemoreceptor input to respiratory hypoglossal motoneurons." Journal of Applied Physiology 69, no. 2 (August 1, 1990): 700–709. http://dx.doi.org/10.1152/jappl.1990.69.2.700.
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To better understand the role of the arterial chemoreceptors in the regulation of upper airway patency at the level of the oropharynx, intracellular recordings were obtained from inspiratory hypoglossal motoneurons (IHMs), and the responses to selective activation of the carotid body chemoreceptors were examined. In pentobarbital-anesthetized, vagotomized, paralyzed, and artificially ventilated cats, chemoreceptor activation enhanced the inspiratory depolarization of membrane potential in 32 of 36 IHMs. This was manifested as an increase in either the amplitude (n = 13) or duration (n = 3) or an increase in both amplitude and duration (n = 16) of the inspiratory membrane potential depolarization. The amplitude and duration of the inspiratory membrane potential depolarization increased 98 +/- 15% (n = 29) and 78 +/- 13% (n = 19), respectively. Similar patterns of enhanced activity (increased duration and/or amplitude of membrane depolarization) were observed in five expiratory hypoglossal motoneurons (EHMs) after chemoreceptor activation. In 16 of the 32 IHMs, chemoreceptor activation also evoked changes in IHM membrane potential during expiration: enhanced post-inspiratory discharge (n = 6), expiratory depolarization/discharge (n = 6), and tonic depolarization/discharge, which persisted for several respiratory cycles (n = 4). The arterial chemoreceptors provide a powerful excitatory input to IHMs during both inspiration and expiration. This excitatory drive to IHMs and EHMs will aid in the maintenance of upper airway patency throughout the respiratory cycle during increases in end-tidal CO2.
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Reddy, Maram K., Kaushik P. Patel, and Harold D. Schultz. "Differential role of the paraventricular nucleus of the hypothalamus in modulating the sympathoexcitatory component of peripheral and central chemoreflexes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 3 (September 2005): R789—R797. http://dx.doi.org/10.1152/ajpregu.00222.2005.
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In the present study we investigated the involvement of the hypothalamic paraventricular nucleus (PVN) in the modulation of sympathoexcitatory reflex activated by peripheral and central chemoreceptors. We measured mean arterial blood pressure (MAP), heart rate (HR), renal sympathetic nerve activity (RSNA), and phrenic nerve activity (PNA) before and after blocking neurotransmission within the PVN by bilateral microinjection of 2% lidocaine (100 nl) during specific stimulation of peripheral chemoreceptors by potassium cyanide (KCN, 75 μg/kg iv, bolus dose) or stimulation of central chemoreceptors with hypercapnia (10% CO2). Typically stimulation of peripheral chemoreceptors evoked a reflex response characterized by an increase in MAP, RSNA, and PNA and a decrease in HR. Bilateral microinjection of 2% lidocaine into the PVN had no effect on basal sympathetic and cardiorespiratory variables; however, the RSNA and PNA responses evoked by peripheral chemoreceptor stimulation were attenuated ( P < 0.05). Bilateral microinjection of bicuculline (50 pmol/50 nl, n = 5) into the PVN augmented the RSNA and PNA response to peripheral chemoreceptor stimulation ( P < 0.05). Conversely, the GABA agonist muscimol (0.2 nmol/50 nl, n = 5) injected into the PVN attenuated these reflex responses ( P < 0.05). Blocking neurotransmission within the PVN had no effect on the hypercapnia-induced central chemoreflex responses in carotid body denervated animals. These results suggest a selective role of the PVN in processing the sympathoexcitatory and ventilatory component of the peripheral, but not central, chemoreflex.
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Hayward, L. F., and R. B. Felder. "Peripheral chemoreceptor inputs to the parabrachial nucleus of the rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 3 (March 1, 1995): R707—R714. http://dx.doi.org/10.1152/ajpregu.1995.268.3.r707.
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In the urethan-anesthetized rat, extracellular recordings were made from 60 neurons within the region of the parabrachial nucleus (PBN). The activity of 37 of 44 neurons was altered by selective stimulation of peripheral chemoreceptors via intracarotid injection of NaH2PO4 or CO2-saturated NaHCO3. Most of these neurons (28 of 37) were excited during chemoreceptor stimulation. Twenty-four of 48 neurons responded to changes in baroreceptor input via changes in blood pressure. Most of these neurons (18 of 24) were inhibited during baroreceptor stimulation. Eleven of 32 neurons were affected by both chemoreceptor and baroreceptor inputs. Seven of these neurons had opposite responses during selective afferent stimulation; that is, they were excited during chemoreceptor activation and inhibited during baroreceptor activation. Our observations reveal that neurons within the medial and lateral PBN are responsive to peripheral chemoreceptor input. A subgroup of PBN neurons was shown to integrate information from chemoreceptors and baroreceptors. These results suggest that both the medial and lateral PBN may play a role in the central integration of cardiovascular inputs.
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Haibara, A. S., E. Colombari, D. A. Chianca, L. G. Bonagamba, and B. H. Machado. "NMDA receptors in NTS are involved in bradycardic but not in pressor response of chemoreflex." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 4 (October 1, 1995): H1421—H1427. http://dx.doi.org/10.1152/ajpheart.1995.269.4.h1421.
Full textAbstract:
Activation of carotid chemoreceptors with intravenous potassium cyanide (KCN) produces increases in arterial pressure, bradycardia, and tachypnea. In the present study, we activated carotid chemoreceptors with KCN and the neurotransmission of the chemoreceptor reflex into the commissural nucleus tractus solitarii (NTS) was blocked with phosphonovaleric acid (AP-5), an N-methyl-D-aspartate (NMDA)-selective antagonist. The aim of this study was to evaluate the involvement of NMDA receptors in the cardiovascular and respiratory responses produced by chemoreceptor activation in unanesthetized rats. The pressor response to KCN was not changed after microinjection of three different doses of AP-5 into the NTS, whereas the bradycardic response was reduced in a dose-dependent manner. The increase in respiratory frequency in response to carotid chemoreceptor activation was also not affected by AP-5 microinjected into the NTS. The data indicate that the activation of the cardiovagal component of the chemoreflex in the commissural NTS is mediated by NMDA receptors, whereas pressor and ventilatory responses are not.
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Tominaga, Masamune, Thomas A. Stekiel, Zeljko J. Bosnjak, and John P. Kampine. "Contribution of carotid chemoreceptors to mesenteric venoconstriction during acute hypercapnia in rabbits." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 6 (December 1, 1999): H2305—H2310. http://dx.doi.org/10.1152/ajpheart.1999.277.6.h2305.
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The contribution of carotid chemoreceptors to hypercapnia-induced mesenteric venoconstriction was examined in 12 α-chloralose-anesthetized rabbits (1.0–1.6 kg). Surgical preparation consisted of a tracheotomy, femoral arterial and venous cannulation, and a midline laparotomy through which a 13-cm loop of ileum was exteriorized and superfused with physiological salt solution. Mesenteric vein diameter and intravenous pressure (using a servo-null measurement system) were measured in 500- to 1,000-μm mesenteric veins during 40-s periods of 15%, 20%, and 25% CO2 inhalation. Measurements were then repeated following bilateral ablation of the carotid chemoreceptors. Before denervation, mesenteric vein diameter constricted 6.5 ± 1.1%, 11.9 ± 1.1%, and 17.9 ± 2.2% during the 15%, 20%, and 25% CO2 inhalation, respectively. After denervation, these values were reduced to 5.0 ± 0.9%, 6.9 ± 1.2%, and 8.4 ± 1.3%, respectively. We conclude that activation of the carotid chemoreceptors by hypercapnia induces active mesenteric venoconstriction. After denervation of the carotid baroreceptors and chemoreceptors, there was also a small decrease in venule diameter proportional to the level of inspired CO2. We further conclude that noncarotid body chemoreceptor activation contributes to mesenteric venular constriction.
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Parkes, M. J. "Evaluating the Importance of the Carotid Chemoreceptors in Controlling Breathing during Exercise in Man." BioMed Research International 2013 (2013): 1–18. http://dx.doi.org/10.1155/2013/893506.
Full textAbstract:
Only the carotid chemoreceptors stimulate breathing during hypoxia in Man. They are also ideally located to warn if the brain’s oxygen supply falls, or if hypercapnia occurs. Since their discovery ~80 years ago stimulation, ablation, and recording experiments still leave 3 substantial difficulties in establishing how important the carotid chemoreceptors are in controlling breathing during exercise in Man: (i) they are in the wrong location to measure metabolic rate (but are ideally located to measure any mismatch), (ii) they receive no known signal during exercise linking them with metabolic rate and no overt mismatch signals occur and (iii) their denervation in Man fails to prevent breathing matching metabolic rate in exercise. New research is needed to enable recording from carotid chemoreceptors in Man to establish whether there is any factor that rises with metabolic rate and greatly increases carotid chemoreceptor activity during exercise. Available evidence so far in Man indicates that carotid chemoreceptors are either one of two mechanisms that explain breathing matching metabolic rate or have no importance. We still lack key experimental evidence to distinguish between these two possibilities.
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Forster, H. V., and C. A. Smith. "Contributions of central and peripheral chemoreceptors to the ventilatory response to CO2/H+." Journal of Applied Physiology 108, no. 4 (April 2010): 989–94. http://dx.doi.org/10.1152/japplphysiol.01059.2009.
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The major objective of this review is to evaluate existing information and reach conclusions regarding whether there is interaction between Pco2/H+ stimulation of carotid (peripheral) and intracranial (central) chemoreceptors. Interaction is defined as a ventilatory response to simultaneous changes in the degree of Pco2/H+ stimulation of both chemoreceptors that is greater (hyperadditive) or less (hypoadditive) than the sum of the responses when stimulation of each set of chemoreceptors is individually altered. Simple summation of the simultaneous changes in stimuli results in no interaction (i.e., additive interaction). Knowledge of the nature of central/peripheral interaction is crucial for determining the physiological significance of newer models of ventilatory control based on recent neuroanatomic observations of the circuitry of key elements of the ventilatory control system. In this review, we will propose that these two sets of receptors are not functionally separate but rather that they are dependent on one another such that the sensitivity of the medullary chemoreceptors is critically determined by input from the peripheral chemoreceptors and possibly other breathing-related reflex afferents as well. The short format of this minireview demands that we be somewhat selective in developing our ideas. We will briefly discuss the limitations of experiments used to study CO2/H+ sensitivity and interaction to date, traditional views of the relative contributions of peripheral and central chemoreceptors to CO2/H+ sensitivity, the evidence for and against different types of interaction, and the effect of tonic carotid chemoreceptor afferent activity on central control mechanisms.
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Lamanna, Allison C., Jason E. Gestwicki, Laura E. Strong, Sara L. Borchardt, Robert M. Owen, and Laura L. Kiessling. "Conserved Amplification of Chemotactic Responses through Chemoreceptor Interactions." Journal of Bacteriology 184, no. 18 (September 15, 2002): 4981–87. http://dx.doi.org/10.1128/jb.184.18.4981-4987.2002.
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ABSTRACT Many bacteria concentrate their chemoreceptors at the cell poles. Chemoreceptor location is important in Escherichia coli, since chemosensory responses are sensitive to receptor proximity. It is not known, however, whether chemotaxis in other bacteria is similarly regulated. To investigate the importance of receptor-receptor interactions in other bacterial species, we synthesized saccharide-bearing multivalent ligands that are designed to cluster relevant chemoreceptors. As has been shown with E. coli, we demonstrate that the behaviors of Bacillus subtilis, Spirochaete aurantia, and Vibrio furnissii are sensitive to the valence of the chemoattractant. Moreover, in B. subtilis, chemotactic responses to serine were increased by pretreatment with saccharide-bearing multivalent ligands. This result indicates that, as in E. coli, signaling information is transferred among chemoreceptors in B. subtilis. These results suggest that interreceptor communication may be a general mechanism for modulating chemotactic responses in bacteria.
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Branco, L. G., and S. C. Wood. "Effect of temperature on central chemical control of ventilation in the alligator Alligator mississippiensis." Journal of Experimental Biology 179, no. 1 (June 1, 1993): 261–72. http://dx.doi.org/10.1242/jeb.179.1.261.
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Central chemoreceptor function was assessed in unanesthetized alligators, Alligator mississippiensis, at body temperatures of 15, 25 and 35 degrees C. Two experiments were performed. In the first experiment, the fourth ventricle was perfused with mock cerebrospinal fluid (CSF) solutions of different pH values (7.1-7.9). Changes in pulmonary ventilation were evaluated with a pneumotachograph and arterial pH (pHa) was measured. Perfusion with low-pH solutions increased ventilation and arterial pH. Perfusion with high-pH solutions decreased ventilation and arterial pH. Mock CSF pH had a greater effect at higher temperatures. In the second experiment, the relative contributions of central and peripheral chemoreceptor drive to breathing were evaluated using hypercapnic gas mixtures to stimulate both central and peripheral chemoreceptors. Hypercapnia caused an increase in ventilation which was larger at higher temperatures. To stimulate only the peripheral chemoreceptors, the same hypercapnic gas mixtures were applied while the CSF pH of the fourth ventricle was kept constant by perfusion with a mock CSF solution. This reduced significantly the ventilatory response induced by hypercapnia. These data indicate that, regardless of the temperature, central chemoreceptors play a major role in the ventilatory regulation of the alligator. The change in pHa with temperature is compatible with the alphastat hypothesis.
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Stalla, David, Narahari Akkaladevi, Tommi White, and Gerald Hazelbauer. "Spatial Restrictions in Chemotaxis Signaling Arrays: A Role for Chemoreceptor Flexible Hinges across Bacterial Diversity." International Journal of Molecular Sciences 20, no. 12 (June 19, 2019): 2989. http://dx.doi.org/10.3390/ijms20122989.
Full textAbstract:
The chemotactic sensory system enables motile bacteria to move toward favorable environments. Throughout bacterial diversity, the chemoreceptors that mediate chemotaxis are clustered into densely packed arrays of signaling complexes. In these arrays, rod-shaped receptors are in close proximity, resulting in limited options for orientations. A recent geometric analysis of these limitations in Escherichia coli, using published dimensions and angles, revealed that in this species, straight chemoreceptors would not fit into the available space, but receptors bent at one or both of the recently-documented flexible hinges would fit, albeit over a narrow window of shallow bend angles. We have now expanded our geometric analysis to consider variations in receptor length, orientation and placement, and thus to species in which those parameters are known to be, or might be, different, as well as to the possibility of dynamic variation in those parameters. The results identified significant limitations on the allowed combinations of chemoreceptor dimensions, orientations and placement. For most combinations, these limitations excluded straight chemoreceptors, but allowed receptors bent at a flexible hinge. Thus, our analysis identifies across bacterial diversity a crucial role for chemoreceptor flexible hinges, in accommodating the limitations of molecular crowding in chemotaxis core signaling complexes and their arrays.
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Lahiri, S., C. Hsiao, R. Zhang, A. Mokashi, and T. Nishino. "Peripheral chemoreceptors in respiratory oscillations." Journal of Applied Physiology 58, no. 6 (June 1, 1985): 1901–8. http://dx.doi.org/10.1152/jappl.1985.58.6.1901.
Full textAbstract:
The hypothesis that instability of cardiorespiratory control may depend on the response and sensitivity of carotid body chemoreceptors to arterial blood gases was studied in anesthetized cats under three different experimental conditions. 1) Following administration of the peripheral dopamine receptor blocker [domperidone (0.6–0.8 mg X kg-1, iv)], carotid chemoreceptor activity and its sensitivity to CO2 during hypoxia increased, leading to cardiorespiratory oscillations at low arterial PO2 in four of eight cats. Inhalation of 100% O2 promptly decreased chemoreceptor activity and eliminated the oscillations. Inhalation of CO2 stimulated the chemoreceptor activity and ventilation but did not eliminate the oscillations. Bilateral section of carotid sinus nerves abolished the cardiorespiratory oscillations. The implication is that the dopaminergic system in the carotid body keeps chemoreceptor responses to blood gas stimuli suppressed and hence cardiorespiratory oscillations damped. 2) Hypotension and circulatory delay induced by the partial occlusion of venous return led to cardiorespiratory oscillations at low but not at high arterial PO2. 3) A few cats developed cardiorespiratory oscillations without any particular experimental intervention. These oscillations were independent of arterial PO2 and chemoreceptor activity. Thus it is reasonable to conclude that the peripheral chemoreflex can play a critical role in developing cardiorespiratory oscillations in certain instances.
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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.
Full textAbstract:
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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Perez, Eduardo, Haiyan Zheng, and Ann M. Stock. "Identification of Methylation Sites in Thermotoga maritima Chemotaxis Receptors." Journal of Bacteriology 188, no. 11 (June 1, 2006): 4093–100. http://dx.doi.org/10.1128/jb.00181-06.
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ABSTRACT Adaptation in bacterial chemotaxis involves reversible methylation of specific glutamate residues within the cytoplasmic domains of methyl-accepting chemotaxis proteins. The specific sites of methylation in Salmonella enterica and Escherichia coli chemoreceptors, identified 2 decades ago, established a consensus sequence for methylation by methyltransferase CheR. Here we report the in vitro methylation of chemoreceptors from Thermotoga maritima, a hyperthermophile that has served as a useful source of chemotaxis proteins for structural analysis. Sites of methylation have been identified by liquid chromatography-mass spectrometry/mass spectrometry. Fifteen sites of methylation were identified within the cytoplasmic domains of four different T. maritima chemoreceptors. The results establish a consensus sequence for chemoreceptor methylation sites in T. maritima that is distinct from the previously identified consensus sequence for E. coli and S. enterica. These findings suggest that consensus sequences for posttranslational modifications in one organism may not be directly extrapolated to analogous modifications in other bacteria.
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Limberg, Jacqueline K., Blair D. Johnson, Michael T. Mozer, Walter W. Holbein, Timothy B. Curry, Nanduri R. Prabhakar, and Michael J. Joyner. "Role of the carotid chemoreceptors in insulin-mediated sympathoexcitation in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 318, no. 1 (January 1, 2020): R173—R181. http://dx.doi.org/10.1152/ajpregu.00257.2019.
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We examined the contribution of the carotid chemoreceptors to insulin-mediated increases in muscle sympathetic nerve activity (MSNA) in healthy humans. We hypothesized that reductions in carotid chemoreceptor activity would attenuate the sympathoexcitatory response to hyperinsulinemia. Young, healthy adults (9 male/9 female, 28 ± 1 yr, 24 ± 1 kg/m2) completed a 30-min euglycemic baseline followed by a 90-min hyperinsulinemic (1 mU·kg fat-free mass−1·min−1), euglycemic infusion. MSNA (microneurography of the peroneal nerve) was continuously measured. The role of the carotid chemoreceptors was assessed at baseline and during hyperinsulinemia via 1) acute hyperoxia, 2) low-dose dopamine (1–4 µg·kg−1·min−1), and 3) acute hyperoxia + low-dose dopamine. MSNA burst frequency increased from baseline during hyperinsulinemia ( P < 0.01). Acute hyperoxia had no effect on MSNA burst frequency at rest ( P = 0.74) or during hyperinsulinemia ( P = 0.83). The insulin-mediated increase in MSNA burst frequency ( P = 0.02) was unaffected by low-dose dopamine ( P = 0.60). When combined with low-dose dopamine, acute hyperoxia had no effect on MSNA burst frequency at rest ( P = 0.17) or during hyperinsulinemia ( P = 0.85). Carotid chemoreceptor desensitization in young, healthy men and women does not attenuate the sympathoexcitatory response to hyperinsulinemia. Our data suggest that the carotid chemoreceptors do not contribute to acute insulin-mediated increases in MSNA in young, healthy adults.
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Li, Aihua, Margaret Randall, and Eugene E. Nattie. "CO2 microdialysis in retrotrapezoid nucleus of the rat increases breathing in wakefulness but not in sleep." Journal of Applied Physiology 87, no. 3 (September 1, 1999): 910–19. http://dx.doi.org/10.1152/jappl.1999.87.3.910.
Full textAbstract:
Central chemoreceptors are widespread within the brain stem. We suggest that their function at some sites may vary with the state of arousal. In this study, we tested the hypothesis that the function of chemoreceptors in the retrotrapezoid nucleus (RTN) varies with sleep and wakefulness. In unanesthetized rats, we produced focal acidification of the RTN by means of a microdialysis probe (tip containing the semipermeable membrane = 1-mm length, 240-μm diameter, and 45-nl volume). With the use of a dialysate equilibrated with 25% CO2, the tissue pH change (measured in anesthetized animals) was 1) limited to within 550 μm of the probe and, 2) at the probe tip, was equivalent to that observed with end-tidal[Formula: see text] of 63 Torr. This focal acidification of the RTN increased ventilation significantly by 24% above baseline, on average, in 13 trials in seven rats only during wakefulness. The effect was entirely due to an increase in tidal volume. During sleep defined by behavioral criteria, ventilation was unaffected, on average, in 10 trials in seven rats. During sleep, the chemoreceptors in the RTN appear to be inactive, or, if active, the respiratory control system either is not responding or is responding with very low gain. Because ventilation is increased during sleep with all central chemoreceptor sites stimulated via systemic CO2 application, other central chemoreceptor locations must have enhanced effectiveness.
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Di Giulio, C., W. X. Huang, S. Lahiri, A. Mokashi, and D. G. Buerk. "Cobalt stimulates carotid body chemoreceptors." Journal of Applied Physiology 68, no. 5 (May 1, 1990): 1844–49. http://dx.doi.org/10.1152/jappl.1990.68.5.1844.
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Because cobalt administration is known to elicit erythropoietin response, it is a reasonable hypothesis that cobalt would also stimulate the O2-sensing process in the peripheral chemoreceptors. We tested this hypothesis by measuring the effects of cobalt chloride on carotid chemosensory fibers in pentobarbital-anesthetized cats that were paralyzed and artificially ventilated. Responses of carotid chemoreceptor afferents to graded doses of cobalt given by intra-arterial injections (0.08-2.10 mumols) were measured at constant blood gases. Responses of the same chemoreceptor afferents to hypoxia, before and after a saturation dose of cobalt, were measured. In two experiments carotid body tissue PO2 was also simultaneously measured. The chemosensory fibers showed prolonged excitation after a brief period of inhibition subsequent to cobalt administration. The stimulatory effect showed a dose-dependent saturation response. Cobalt augmented rather than blocked carotid chemoreceptor response to hypoxia. The effect of cobalt was not mediated by tissue PO2. These results are consistent with the hypothesis that cobalt stimulates the O2-sensing mechanism, although a direct effect of cobalt on the excitability of the chemosensory terminal remains a possibility.
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Xie, Zhihong, Luke E. Ulrich, Igor B. Zhulin, and Gladys Alexandre. "PAS domain containing chemoreceptor couples dynamic changes in metabolism with chemotaxis." Proceedings of the National Academy of Sciences 107, no. 5 (January 19, 2010): 2235–40. http://dx.doi.org/10.1073/pnas.0910055107.
Full textAbstract:
Chemoreceptors provide sensory specificity and sensitivity that enable motile bacteria to seek optimal positions for growth and metabolism in gradients of various physicochemical cues. Despite the abundance of chemoreceptors, little is known regarding the sensory specificity and the exact contribution of individual chemoreceptors to the lifestyle of bacteria. Azospirillum brasilense are motile bacteria that can fix atmospheric nitrogen under microaerophilic conditions. Here, we characterized a chemoreceptor in this organism, named AerC, which functions as a redox sensor that enables the cells to seek microaerophilic conditions that support optimum nitrogen fixation. AerC is a representative of a widespread class of soluble chemoreceptors that monitor changes in the redox status of the electron transport system via the FAD cofactor associated with its PAS domains. In A. brasilense, AerC clusters at the cell poles. Its cellular localization and contribution to the behavioral response correlate with its expression pattern and with changes in the overall cellular FAD content under nitrogen-fixing conditions. AerC-mediated energy taxis in A. brasilense prevails under conditions of nitrogen fixation, illustrating a strategy by which cells optimize chemosensing to signaling cues that directly affect current metabolic activities and thus revealing a mechanism by which chemotaxis is coordinated with dynamic changes in cell physiology.
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Burleson, M. L., and W. K. Milsom. "Propranolol inhibits O2-sensitive chemoreceptor activity in trout gills." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 4 (April 1, 1990): R1089—R1091. http://dx.doi.org/10.1152/ajpregu.1990.258.4.r1089.
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The effects of propranolol on the activity of O2-sensitive chemoreceptors innervated by cranial nerve IX were studied using an isolated, perfused first gill arch preparation from rainbow trout (Onchyrhyncos mykiss). Perfusing the gill with hypoxic perfusate resulted in an increase in chemoreceptor activity. Propranolol (100-200 nmol) added to the perfusate inhibited O2-receptor discharge during both normoxia and hypoxia and attenuated the response to bolus injections of NaCN (25 micrograms). These results suggest that a beta-adrenergic mechanism is involved in O2 chemoreception. They further suggest that the inhibitory effects of propranolol on branchial, O2-sensitive chemoreceptors may contribute to the attenuated hypoxic ventilatory reflex observed in intact fish after propranolol injections.
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Wang, Hao, Mengqi Zhang, Yujuan Xu, Renjie Zong, Nan Xu, and Minliang Guo. "Agrobacterium fabrumatu0526-Encoding Protein Is the Only Chemoreceptor That Regulates Chemoattraction toward the Broad Antibacterial Agent Formic Acid." Biology 10, no. 12 (December 17, 2021): 1345. http://dx.doi.org/10.3390/biology10121345.
Full textAbstract:
Soil-born plant pathogens, especially Agrobacterium, generally navigate their way to hosts through recognition of the root exudates by chemoreceptors. However, there is still a lack of appropriate identification of chemoreceptors and their ligands in Agrobacterium. Here, Atu0526, a sCache-type chemoreceptor from Agrobacterium fabrum C58, was confirmed as the receptor of a broad antibacterial agent, formic acid. The binding of formic acid to Atu0526 was screened using a thermo shift assay and verified using isothermal titration calorimetry. Inconsistent with the previously reported antimicrobial properties, formic acid was confirmed to be a chemoattractant to A. fabrum and could promote its growth. The chemotaxis of A. fabrum C58 toward formic acid was completely lost with the knock-out of atu0526, and regained with the complementation of the gene, indicating that Atu0526 is the only chemoreceptor for formic acid in A. fabrum C58. The affinity of formic acid to Atu0526LBD significantly increased after the arginine at position 115 was replaced by alanine. However, in vivo experiments showed that the R115A mutation fully abolished the chemotaxis of A. fabrum toward formic acid. Molecular docking based on a predicted 3D structure of Atu0526 suggested that the arginine may provide “an anchorage” for formic acid to pull the minor loop, thereby forming a conformational change that generates the ligand-binding signal. Collectively, our findings will promote an understanding of sCache-type chemoreceptors and their signal transduction mechanism.
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TIMMERS, Henri J. L. M., Gerard A. RONGEN, John M. KAREMAKER, Wouter WIELING, Henri A. M. MARRES, and Jacques W. M. LENDERS. "The role of carotid chemoreceptors in the sympathetic activation by adenosine in humans." Clinical Science 106, no. 1 (January 1, 2004): 75–82. http://dx.doi.org/10.1042/cs20030174.
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The direct vasodilatory and negative chronotropic effects of adenosine in humans are counterbalanced by a reflex increase in sympathetic nerve traffic. A suggested mechanism for this reflex includes peripheral chemoreceptor activation. We, therefore, assessed the contribution of carotid chemoreceptors to sympatho-excitation by adenosine. Muscle sympathetic nerve activity was recorded during adenosine infusion (140 µg·kg-1·min-1 for 5 min) in five patients lacking carotid chemoreceptors after bilateral carotid body tumour resection (one male and four female, mean age 51±11 years) and in six healthy controls (two male and four female, mean age 50±7 years). Sympathetic responses to sodium nitroprusside injections were assessed to measure baroreceptor-mediated sympathetic activation. In response to adenosine, controls showed no change in blood pressure, an increase in heart rate (+48.2±13.2%; P<0.003) and an increase in sympathetic nerve activity (+195±103%; P<0.022). In contrast, patients showed a decrease in blood pressure (-14.6±4.9/-17.6±6.0%; P<0.05), an increase in heart rate (+25.3±8.4%; P<0.032) and no significant change in sympathetic activity. Adenosine-induced hypotension in individual patients elicited less sympathetic activation than equihypotensive sodium nitroprusside injections. In humans lacking carotid chemoreceptors, adenosine infusion elicits hypotension due to the absence of significant sympatho-excitation. Chemoreceptor activation is essential for counterbalancing the direct vasodilation by adenosine. In addition, blunting of the baroreflex sympathetic response to adenosine-induced hypotension may indicate a direct sympatho-inhibitory effect of adenosine.
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McCulloch, P. F., and N. H. West. "Cardiovascular responses to nasal water flow in rats are unaffected by chemoreceptor drive." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 5 (November 1, 1992): R1049—R1056. http://dx.doi.org/10.1152/ajpregu.1992.263.5.r1049.
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Peripheral chemoreceptors generally play a limited role in the initial development of diving bradycardia in mammals. However, T.F. Huang and Y.I. Peng (Jpn. J. Physiol. 26: 395-401, 1976) reported that peripheral chemoreceptors are very important for manifestation of the diving response in conscious rats. The objectives of this study were to reinvestigate those findings and determine whether the cardiovascular responses to simulated diving in the rat were potentiated during preexisting hypoxia or hypercapnia. Responses to simulated diving were elicited by nasal water flow with concurrent apnea in paralyzed, artificially ventilated Sprague-Dawley rats anesthetized with Innovar. The experiments show that nasal stimulation in the rat results in rapid bradycardia and hypotension and that these responses are not due to laryngeal stimulation. The data also suggest that chemoreceptors do not play a role in the initiation of the responses to simulated diving in rats and that preexisting chemoreceptor drive does not alter the cardiovascular responses. Additionally, we found that concomitant expiratory apnea is necessary to sustain the profound initial cardiovascular changes induced by nasal water flow.
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Honig, A. "Peripheral arterial chemoreceptors and reflex control of sodium and water homeostasis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 6 (December 1, 1989): R1282—R1302. http://dx.doi.org/10.1152/ajpregu.1989.257.6.r1282.
Full textAbstract:
In response to acute exposure to moderate high-altitude hypoxia, mammals increase their blood hemoglobin concentration very rapidly by reducing their plasma volume. This phenomenon is caused not only by a redistribution of the body fluid volumes but also by a suppression of voluntary sodium and water intake as well as an inhibition of renal tubular sodium reabsorption with natriuresis and diuresis. This article reviews the role of the peripheral arterial chemoreceptors within the framework of the reflex mechanisms that might cause the changes in sodium and water metabolism in acute arterial hypoxia. The evidence that the peripheral arterial chemoreceptors do also influence sodium and water homeostasis in normoxia is presented. The interrelations between carotid body structure and arterial chemoreceptor reflex effects on the one hand and primary systemic hypertension on the other are discussed.
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Barnard, P., S. Andronikou, M. Pokorski, N. Smatresk, A. Mokashi, and S. Lahiri. "Time-dependent effect of hypoxia on carotid body chemosensory function." Journal of Applied Physiology 63, no. 2 (August 1, 1987): 685–91. http://dx.doi.org/10.1152/jappl.1987.63.2.685.
Full textAbstract:
The time-dependent effects of hypoxia on the discharge rate carotid chemoreceptors were measured in anesthetized cats. Hypoxic exposure of two different durations were used: a short-term exposure (2–3 h) was used to measure the response of the same carotid chemoreceptors; and a long-term exposure (28 days at inspired PO2 of 70 Torr) to study carotid chemoreceptor properties in one group of cats relative to those of a control group. In the chronically hypoxic and control groups, determinations were made of the 1) steady-state responses to four levels of arterial PO2 (PaO2) at constant levels of arterial PCO2; 2) steady-state responses to acute hypercapnia during hyperoxia; and 3) maximal discharge rates during anoxia. We found that the acute responses of carotid chemoreceptor afferents to a given level of hypoxia (PaO2 = 30–40 Torr) did not significantly change within 2–3 h. After long-term exposure the carotid chemoreceptor responses to hypoxia significantly increased, with no significant changes in the hypercapnic response and in the maximal discharge rate during anoxia. We conclude that isocapnic hypoxia may not elicit a sufficient cellular response within 2–3 h in the cat carotid body to sensitize the O2 responsive mechanism, but hypoxia of longer duration will sensitize such a mechanism, thereby augmenting the chemosensory activity.
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Iwama, Tomonori, Ko-Ichiro Nakao, Hiroshi Nakazato, Shuzo Yamagata, Michio Homma, and Ikuro Kawagishi. "Mutational Analysis of Ligand Recognition by Tcp, the Citrate Chemoreceptor of Salmonella entericaSerovar Typhimurium." Journal of Bacteriology 182, no. 5 (March 1, 2000): 1437–41. http://dx.doi.org/10.1128/jb.182.5.1437-1441.2000.
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ABSTRACT The chemoreceptor Tcp mediates taxis to citrate. To identify citrate-binding residues, we substituted cysteine for seven basic or polar residues that are chosen based on the comparison of Tcp with the well-characterized chemoreceptors. The results suggest that Arg-63, Arg-68, Arg-72, Lys-75, and Tyr-150 (and probably other unidentified residues) are involved in the recognition of citrate.
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Blum, Daniel J., and Thomas V. McCaffrey. "Effect of Maturation on the Sensitivity of Laryngeal Resistance to Chemoreceptor Stimulation in the Dog." Otolaryngology–Head and Neck Surgery 93, no. 3 (June 1985): 351–54. http://dx.doi.org/10.1177/019459988509300312.
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The respiratory system undergoes many changes with maturation, resulting in increased capacity and efficiency. In an effort to determine the effects of maturation on airway control, laryngeal airway resistance was studied from infancy to adulthood in dogs. Reflex regulation of laryngeal airway resistance in response to chemoreceptor stimulation was found in puppies 1 day of age and older. Chemoreceptor-mediated laryngeal reflexes were qualitatively similar in all age groups. However, a significant quantitative difference was found. With maturation, an increase in the sensitivity of both central and peripheral chemoreceptors regulating laryngeal resistance is realized.
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Abedrabbo, Samar, Juan Castellon, Kieran D. Collins, Kevin S. Johnson, and Karen M. Ottemann. "Cooperation of two distinct coupling proteins creates chemosensory network connections." Proceedings of the National Academy of Sciences 114, no. 11 (February 27, 2017): 2970–75. http://dx.doi.org/10.1073/pnas.1618227114.
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Although it is appreciated that bacterial chemotaxis systems rely on coupling, also called scaffold, proteins to both connect input receptors with output kinases and build interkinase connections that allow signal amplification, it is not yet clear why many systems use more than one coupling protein. We examined the distinct functions for multiple coupling proteins in the bacterial chemotaxis system of Helicobacter pylori, which requires two nonredundant coupling proteins for chemotaxis: CheW and CheV1, a hybrid of a CheW and a phosphorylatable receiver domain. We report that CheV1 and CheW have largely redundant abilities to interact with chemoreceptors and the CheA kinase, and both similarly activated CheA’s kinase activity. We discovered, however, that they are not redundant for formation of the higher order chemoreceptor arrays that are known to form via CheA–CheW interactions. In support of this possibility, we found that CheW and CheV1 interact with each other and with CheA independent of the chemoreceptors. Therefore, it seems that some microbes have modified array formation to require CheW and CheV1. Our data suggest that multiple coupling proteins may be used to provide flexibility in the chemoreceptor array formation.
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Mifflin, S. W. "Arterial chemoreceptor input to nucleus tractus solitarius." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 2 (August 1, 1992): R368—R375. http://dx.doi.org/10.1152/ajpregu.1992.263.2.r368.
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The arterial chemoreceptors play an important role in the reflex regulation of blood pressure and respiration. To investigate the initial integration of chemoreceptor inputs within the central nervous system, intracellular recordings were obtained in pentobarbital-anesthetized, paralyzed, and mechanically ventilated cats, from 58 cells within the nucleus of the tractus solitarius (NTS) that were depolarized by activation of the ipsilateral carotid body chemoreceptors. Close arterial injection of less than 100 microliters CO2-saturated bicarbonate evoked depolarizations of membrane potential with amplitudes of 2.2-4.6 mV and durations of 1.8-6.7 s in 46 cells. In 12 cells, activation of the carotid body chemoreceptors evoked a depolarization-hyperpolarization sequence. Electrical stimulation of the carotid sinus nerve (500 microA, 0.2 ms) evoked EPSPs [mean latency 6.4 +/- 0.5 (SE) ms; range 2.1-18.4 ms] in 46 cells and EPSP-IPSPs (7.3 +/- 0.8 ms; range 4.2-12.4 ms) in 12 cells. The distribution of EPSP latencies exhibited two peaks, one in the 2- to 4-ms range and another in the 7- to 8-ms range. Twenty-nine chemoreceptive cells were tested for the presence of convergent inputs from the ipsilateral carotid sinus baroreceptors. No evidence was found of a convergent postsynaptic inhibitory input from the baroreceptors within the NTS; however, seven cells were found that received an excitatory input from the baroreceptors. The observation that NTS neurons do not integrate chemoreceptor afferent inputs in a homogeneous manner suggests that the multiplicity of NTS unit responses might be related to the specific reflex function of an individual cell (e.g., vagal or sympathetic outflow, respiration).(ABSTRACT TRUNCATED AT 250 WORDS)
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Hickner, Paul V., Nataliya Timoshevskaya, Ronald J. Nowling, Frédéric Labbé, Andrew D. Nguyen, Mary Ann McDowell, Carolina N. Spiegel, and Zainulabeuddin Syed. "Molecular signatures of sexual communication in the phlebotomine sand flies." PLOS Neglected Tropical Diseases 14, no. 12 (December 28, 2020): e0008967. http://dx.doi.org/10.1371/journal.pntd.0008967.
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Phlebotomine sand flies employ an elaborate system of pheromone communication wherein males produce pheromones that attract other males to leks (thus acting as an aggregation pheromone) and females to the lekking males (sex pheromone). In addition, the type of pheromone produced varies among populations. Despite the numerous studies on sand fly chemical communication, little is known of their chemosensory genome. Chemoreceptors interact with chemicals in an organism’s environment to elicit essential behaviors such as the identification of suitable mates and food sources. Thus, they play important roles during adaptation and speciation. Major chemoreceptor gene families, odorant receptors (ORs), gustatory receptors (GRs) and ionotropic receptors (IRs) together detect and discriminate the chemical landscape. Here, we annotated the chemoreceptor repertoire in the genomes of Lutzomyia longipalpis and Phlebotomus papatasi, major phlebotomine vectors in the New World and Old World, respectively. Comparison with other sequenced Diptera revealed a large and unique expansion where over 80% of the ~140 ORs belong to a single, taxonomically restricted clade. We next conducted a comprehensive analysis of the chemoreceptors in 63 L. longipalpis individuals from four different locations in Brazil representing allopatric and sympatric populations and three sex-aggregation pheromone types (chemotypes). Population structure based on single nucleotide polymorphisms (SNPs) and gene copy number in the chemoreceptors corresponded with their putative chemotypes, and corroborate previous studies that identified multiple populations. Our work provides genomic insights into the underlying behavioral evolution of sexual communication in the L. longipalpis species complex in Brazil, and highlights the importance of accounting for the ongoing speciation in central and South American Lutzomyia that could have important implications for vectorial capacity.
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Feng, Haichao, Nan Zhang, Wenbin Du, Huihui Zhang, Yunpeng Liu, Ruixin Fu, Jiahui Shao, Guishan Zhang, Qirong Shen, and Ruifu Zhang. "Identification of Chemotaxis Compounds in Root Exudates and Their Sensing Chemoreceptors in Plant-Growth-Promoting Rhizobacteria Bacillus amyloliquefaciens SQR9." Molecular Plant-Microbe Interactions® 31, no. 10 (October 2018): 995–1005. http://dx.doi.org/10.1094/mpmi-01-18-0003-r.
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Chemotaxis-mediated response to root exudates, initiated by sensing-specific ligands through methyl-accepting chemotaxis proteins (MCP), is very important for root colonization and beneficial functions of plant-growth-promoting rhizobacteria (PGPR). Systematic identification of chemoattractants in complex root exudates and their sensing chemoreceptors in PGPR is helpful for enhancing their recruitment and colonization. In this study, 39 chemoattractants and 5 chemorepellents, including amino acids, organic acids, and sugars, were identified from 98 tested components of root exudates for the well-studied PGPR strain Bacillus amyloliquefaciens SQR9. Interestingly, mutant stain SQR9Δ8mcp, with all eight putative chemoreceptors completely deleted, lost the chemotactic responses to those 44 compounds. Gene complementation, chemotaxis assay, and isothermal titration calorimetry analysis revealed that McpA was mainly responsible for sensing organic acids and amino acids, while McpC was mostly for amino acids. These two chemoreceptors may play important roles in the rhizosphere chemotaxis of SQR9. In contrast, the B. amyloliquefaciens-unique chemoreceptor McpR was specifically responsible for arginine, and residues Tyr-78, Thr-131, and Asp-162 were critical for arginine binding. This study not only deepened our insights into PGPR–root interaction but also provided useful information to enhance the rhizosphere chemotaxis mobility and colonization of PGPR, which will promote their application in agricultural production.
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Fujii, Naoto, Miki Kashihara, Glen P. Kenny, Yasushi Honda, Tomomi Fujimoto, Yinhang Cao, and Takeshi Nishiyasu. "Carotid chemoreceptors have a limited role in mediating the hyperthermia-induced hyperventilation in exercising humans." Journal of Applied Physiology 126, no. 2 (February 1, 2019): 305–13. http://dx.doi.org/10.1152/japplphysiol.00562.2018.
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Hyperthermia causes hyperventilation at rest and during exercise. We previously reported that carotid chemoreceptors partly contribute to the hyperthermia-induced hyperventilation at rest. However, given that a hyperthermia-induced hyperventilation markedly differs between rest and exercise, the results obtained at rest may not be representative of the response in exercise. Therefore, we evaluated whether carotid chemoreceptors contribute to hyperthermia-induced hyperventilation in exercising humans. Eleven healthy young men (23 ± 2 yr) cycled in the heat (37°C) at a fixed submaximal workload equal to ~55% of the individual’s predetermined peak oxygen uptake (moderate intensity). To suppress carotid chemoreceptor activity, 30-s hyperoxia breathing (100% O2) was performed at rest (before exercise) and during exercise at increasing levels of hyperthermia as defined by an increase in esophageal temperature of 0.5°C (low), 1.0°C (moderate), 1.5°C (high), and 2.0°C (severe) above resting levels. Ventilation during exercise gradually increased as esophageal temperature increased (all P ≤ 0.05), indicating that hyperthermia-induced hyperventilation occurred. Hyperoxia breathing suppressed ventilation in a greater manner during exercise (−9 to −13 l/min) than at rest (−2 ± 1 l/min); however, the magnitude of reduction during exercise did not differ at low (0.5°C) to severe (2.0°C) increases in esophageal temperature (all P > 0.05). Similarly, hyperoxia-induced changes in ventilation during exercise as assessed by percent change from prehyperoxic levels were not different at all levels of hyperthermia (~15–20%, all P > 0.05). We show that in young men carotid chemoreceptor contribution to hyperthermia-induced hyperventilation is relatively small at low-to-severe increases in body core temperature induced by moderate-intensity exercise in the heat. NEW & NOTEWORTHY Exercise-induced increases in hyperthermia cause a progressive increase in ventilation in humans. However, the mechanisms underpinning this response remain unresolved. We showed that in young men hyperventilation associated with exercise-induced hyperthermia is not predominantly mediated by carotid chemoreceptors. This study provides important new insights into the mechanism(s) underpinning the regulation of hyperthermia-induced hyperventilation in humans and suggests that factor(s) other than carotid chemoreceptors play a more important role in mediating this response.
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Karim, F., and M. al‐Obaidi. "Modification of carotid chemoreceptor‐induced changes in renal haemodynamics and function by carotid baroreflex in dogs." Journal of Physiology 466, no. 1 (July 1993): 599–610. http://dx.doi.org/10.1113/jphysiol.1993.sp019736.
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1. Mongrel dogs were anaesthetized with thiopental sodium and chloralose and artificially ventilated. The carotid sinus regions were vascularly isolated and perfused either with arterial or mixed (arterial and venous) blood (PO2, 44.2 +/‐ 3.3 mmHg, mean +/‐ S.E.M.) to stimulate the chemoreceptors. Cervical vagosympathetic trunks were ligated and atenolol (2 mg kg‐1, I.V.) was given in all dogs and gallamine triethiodide (3 mg kg‐1 h‐1, I.V.) was given in two dogs. Renal blood flow was measured by an electromagnetic flowmeter, glomerular filtration rate by creatinine clearance, sodium excretion by flame photometry and solute excretion by osmometry. The viability of the preparations was tested by recording total vascular capacitance responses to stimulation of carotid baro‐ and chemoreceptors. 2. In eleven tests in seven dogs at a constant aortic pressure of 88.9 +/‐ 2.6 mmHg stimulation of carotid chemoreceptors at a high carotid sinus pressure (194.0 +/‐ 3.6 mmHg) resulted in significant increases in urine flow of 22.8 +/‐ 3.0%, urinary sodium excretion of 30.7 +/‐ 5.2%, fractional sodium excretion of 35.3 +/‐ 18.6%, osmolar excretion of 17.5 +/‐ 4.1% and a decrease in free water clearance of 30.8 +/‐ 3.1% without significant changes in urinary sodium concentration, renal blood flow, glomerular filtration rate, and filtration fraction. 3. In seventeen tests in these seven dogs at a constant aortic pressure of 94.0 +/‐ 2.2 mmHg, stimulation of carotid chemoreceptor at a low carotid sinus pressure (72.0 +/‐ 1.3 mmHg) resulted in significant decreases in renal blood flow of 10.6 +/‐ 2.5%, glomerular filtration rate of 19.6 +/‐ 6.8%, filtration fraction of 13.2 +/‐ 5.5%, urine flow of 23.4 +/‐ 4.1%, urinary sodium concentration of 20.3 +/‐ 4.1%, urinary sodium excretion of 38.5 +/‐ 4.6%, fractional sodium excretion of 20.2 +/‐ 7.7%, osmolar excretion of 23.9 +/‐ 4.0% and an increase in free water clearance of 23.1 +/‐ 2.5%. 4. The results show that moderate stimulation of carotid chemoreceptors at a low carotid sinus pressure, when the activity in renal nerves is high and blood volume is low, can produce significant reflex decreases in renal haemodynamic and functional variables. However, at a high carotid sinus pressure when the renal sympathetic activity is low and blood volume is high, carotid chemoreceptor stimulation produces diuresis and natriuresis but no change in renal haemodynamics.
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Forster, H. V., M. B. Dunning, T. F. Lowry, B. K. Erickson, M. A. Forster, L. G. Pan, A. G. Brice, and R. M. Effros. "Effect of asthma and ventilatory loading on arterial PCO2 of humans during submaximal exercise." Journal of Applied Physiology 75, no. 3 (September 1, 1993): 1385–94. http://dx.doi.org/10.1152/jappl.1993.75.3.1385.
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In humans, attenuating carotid chemoreceptor activity by hyperoxia does not alter arterial PCO2 (PaCO2) during submaximal exercise, yet a transient hypercapnia occurs in carotid chemoreceptor-resected (CBR) asthmatic subjects during submaximal exercise. We hypothesized that this difference was due to asthma and not CBR causing the abnormal response. Accordingly, we determined the temporal pattern of PaCO2 during mild and moderate exercise in chemoreceptor-intact asthmatic (n = 10) and nonasthmatic subjects (n = 10). We also hypothesized that hyperoxia alters PaCO2 during exercise if exercise already has disrupted PaCO2 homeostasis. Accordingly, we studied, during exercise, asthmatic subjects while hyperoxic; nonasthmatic subjects during loaded breathing of room air, which increased PaCO2; and nonasthmatic subjects during loaded breathing while hyperoxic. While breathing room air, neither asthmatic nor nonasthmatic subjects maintained arterial isocapnia during exercise. An increase in PaCO2 between rest and exercise and between mild exercise and 1st min of moderate exercise was greater in asthmatic than in nonasthmatic subjects (P < 0.05). In six asthmatic subjects that were hypercapnic breathing room air during exercise, hypercapnia was accentuated by hyperoxia. The ventilatory load in nonasthmatic subjects resulted in a work load-dependent hypercapnia (P < 0.01) accentuated (P < 0.01) by hyperoxia. We conclude that normally in humans the carotid chemoreceptors contribute minimally to the hyperpnea of submaximal exercise. However, when PaCO2 is increased from resting values during exercise, then the chemoreceptors serve to augment ventilation and thereby minimize the hypercapnia.