Multiple Roles of Neurotransmitters in the Carotid Body: Involvement in Sensory Transmission and Adaptation to Hypoxia

2003 ◽  
pp. 463-479
Keyword(s):  
Carotid Body ◽  
Multiple Roles ◽  
Adaptation To Hypoxia ◽  
Sensory Transmission

scholarly journals Fast neurogenesis from carotid body quiescent neuroblasts accelerates adaptation to hypoxia

EMBO Reports ◽  
2018 ◽  
Vol 19 (3) ◽  
Author(s):  
Verónica Sobrino ◽  
Patricia González‐Rodríguez ◽  
Valentina Annese ◽  
José López‐Barneo ◽  
Ricardo Pardal
Keyword(s):  
Carotid Body ◽  
Adaptation To Hypoxia

scholarly journals Oxygen sensing by the carotid body: mechanisms and role in adaptation to hypoxia

2016 ◽  
Vol 310 (8) ◽  
pp. C629-C642 ◽  
Author(s):  
José López-Barneo ◽  
Patricia González-Rodríguez ◽  
Lin Gao ◽  
M. Carmen Fernández-Agüera ◽  
Ricardo Pardal ◽  
...  
Keyword(s):  
Carotid Body ◽  
Close Contact ◽  
Nerve Fibers ◽  
Whole Body ◽  
Adaptation To Hypoxia ◽  
Glomus Cells ◽  
Adaptive Processes ◽  
Cell Depolarization ◽  
Sensory Fibers

Oxygen (O2) is fundamental for cell and whole-body homeostasis. Our understanding of the adaptive processes that take place in response to a lack of O2 (hypoxia) has progressed significantly in recent years. The carotid body (CB) is the main arterial chemoreceptor that mediates the acute cardiorespiratory reflexes (hyperventilation and sympathetic activation) triggered by hypoxia. The CB is composed of clusters of cells (glomeruli) in close contact with blood vessels and nerve fibers. Glomus cells, the O2-sensitive elements in the CB, are neuron-like cells that contain O2-sensitive K+ channels, which are inhibited by hypoxia. This leads to cell depolarization, Ca2+ entry, and the release of transmitters to activate sensory fibers terminating at the respiratory center. The mechanism whereby O2 modulates K+ channels has remained elusive, although several appealing hypotheses have been postulated. Recent data suggest that mitochondria complex I signaling to membrane K+ channels plays a fundamental role in acute O2 sensing. CB activation during exposure to low Po2 is also necessary for acclimatization to chronic hypoxia. CB growth during sustained hypoxia depends on the activation of a resident population of stem cells, which are also activated by transmitters released from the O2-sensitive glomus cells. These advances should foster further studies on the role of CB dysfunction in the pathogenesis of highly prevalent human diseases.

Oxygen sensing by the carotid body chemoreceptors

2000 ◽  
Vol 88 (6) ◽  
pp. 2287-2295 ◽  
Author(s):  
Nanduri R. Prabhakar
Keyword(s):  
Carotid Body ◽  
Oxygen Sensor ◽  
Oxygen Sensing ◽  
Transgenic Animals ◽  
Sensory Transduction ◽  
Type I ◽  
Cellular Mechanisms ◽  
Arterial Blood ◽  
Sensory Transmission ◽  
Carotid Body Chemoreceptors

Carotid bodies are sensory organs that detect changes in arterial blood oxygen, and the ensuing reflexes are critical for maintaining homeostasis during hypoxemia. During the past decade, tremendous progress has been made toward understanding the cellular mechanisms underlying oxygen sensing at the carotid body. The purpose of this minireview is to highlight some recent concepts on sensory transduction and transmission at the carotid body. A bulk of evidence suggests that glomus (type I) cells are the initial site of transduction and that they release transmitters in response to hypoxia, which causes depolarization of nearby afferent nerve endings, leading to an increase in sensory discharge. There are two main hypotheses to explain the transduction process that triggers transmitter release. One hypothesis assumes that a biochemical event associated with a heme protein triggers the transduction cascade. The other hypothesis suggests that a K+ channel protein is the oxygen sensor and that inhibition of this channel by hypoxia leading to depolarization is a seminal event in transduction. Although there is body of evidence supporting and questioning each of these, this review will try to point out that the truth lies somewhere in an interrelation between the two. Several transmitters have been identified in glomus cells, and they are released in response to hypoxia. However, their precise roles in sensory transmission remain uncertain. It is hoped that future studies involving transgenic animals with targeted disruption of genes encoding transmitters and their receptors may resolve some of the key issues surrounding the sensory transmission at the carotid body. Further studies are necessary to identify whether a single sensor or multiple oxygen sensors are needed for the transduction process.

Carotid body oxygen sensing and adaptation to hypoxia

2015 ◽  
Vol 468 (1) ◽  
pp. 59-70 ◽  
Author(s):  
José López-Barneo ◽  
David Macías ◽  
Aida Platero-Luengo ◽  
Patricia Ortega-Sáenz ◽  
Ricardo Pardal
Keyword(s):  
Carotid Body ◽  
Oxygen Sensing ◽  
Adaptation To Hypoxia

scholarly journals Postsynaptic action of GABA in modulating sensory transmission in co-cultures of rat carotid body via GABAAreceptors

2009 ◽  
Vol 587 (2) ◽  
pp. 329-344 ◽  
Author(s):  
Min Zhang ◽  
Katherine Clarke ◽  
Huijun Zhong ◽  
Cathy Vollmer ◽  
Colin A. Nurse
Keyword(s):  
Carotid Body ◽  
Sensory Transmission ◽  
Postsynaptic Action

Fine Structure of Carotid Body: Normal and Anoxic Cats

1967 ◽  
Vol 25 ◽  
pp. 150-151
Author(s):  
Fadhil Al-Lami ◽  
R.G. Murray
Keyword(s):  
Fine Structure ◽  
Adrenal Medulla ◽  
Carotid Body ◽  
Uranyl Acetate ◽  
Lead Citrate ◽  
Glomus Cells ◽  
Sustentacular Cells ◽  
Carotid Bodies

Although the fine structure of the carotid body has been described in several recent reports, uncertainties remain, and the morphological effects of anoxia on the carotid body cells of the cat have never been reported. We have, therefore, studied the fine structure of the carotid body both in normal and severely anoxic cats, and to test the specificity of the effects, have compared them with the effects on adrenal medulla, kidney, and liver of the same animals. Carotid bodies of 50 normal and 15 severely anoxic cats (9% oxygen in nitrogen) were studied. Glutaraldehyde followed by OsO4 fixations, Epon 812 embedding, and uranyl acetate and lead citrate staining, were the technics employed.We have called the two types of glomus cells enclosed and enclosing cells. They correspond to those previously designated as chemoreceptor and sustentacular cells respectively (1). The enclosed cells forming the vast majority, are irregular in shape with many processes and occasional peripheral densities (Fig. 1).

Microchemistry of ZnO Varistors

1992 ◽  
Vol 50 (2) ◽  
pp. 1694-1695
Author(s):  
K. K. Soni ◽  
J. Hwang ◽  
V. P. Dravid ◽  
T. O. Mason ◽  
R. Levi-Setti
Keyword(s):  
Grain Boundaries ◽  
Multiple Roles ◽  
Grain Boundary Engineering ◽  
Ion Microprobe ◽  
Dopant Distribution ◽  
Important Ingredient ◽  
Zno Varistor ◽  
Zno Varistors ◽  
Zno Powder ◽  
The University

ZnO varistors are made by mixing semiconducting ZnO powder with powders of other metal oxides e.g. Bi2O3, Sb2O3, CoO, MnO2, NiO, Cr2O3, SiO2 etc., followed by conventional pressing and sintering. The non-linear I-V characteristics of ZnO varistors result from the unique properties that the grain boundaries acquire as a result of dopant distribution. Each dopant plays important and sometimes multiple roles in improving the properties. However, the chemical nature of interfaces in this material is formidable mainly because often trace amounts of dopants are involved. A knowledge of the interface microchemistry is an essential component in the ‘grain boundary engineering’ of materials. The most important ingredient in this varistor is Bi2O3 which envelopes the ZnO grains and imparts high resistance to the grain boundaries. The solubility of Bi in ZnO is very small but has not been experimentally determined as a function of temperature.In this study, the dopant distribution in a commercial ZnO varistor was characterized by a scanning ion microprobe (SIM) developed at The University of Chicago (UC) which offers adequate sensitivity and spatial resolution.

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