scholarly journals Immunohistochemical features of the human carotid body

2020 ◽  
Vol 9 (3) ◽  
pp. 61-67
Author(s):  
D.A. Otlyga ◽  
O.A. Junemann ◽  
E.G. Tsvetkova ◽  
K.R. Gorokhov ◽  
S.V. Saveliev
Keyword(s):  
Tyrosine Hydroxylase ◽  
Carotid Body ◽  
Molecular Genetic ◽  
Nerve Fibers ◽  
Laboratory Animals ◽  
Type I ◽  
Nuclear Staining ◽  
Human Organ ◽  
Rats And Mice ◽  
Human Carotid

Introduction. The carotid body is a chemoreceptor organ and the initial link of the reflex regulation of car-diovascular and respiratory systems. However, molecular genetic and immunohistochemical characteristics of the human carotid body remains underinvestigated. Although there are numerous studies of the second half of the 20th century devoted to the classical light-optical histology of the human organ, the immunohis-tochemical investigations are very few. The aim of our study was to clarify immunohistochemical features of the human carotid body in comparison with those of the most commonly used laboratory animals. Materials and methods. The study was performed on 10 carotid bodies of the adult human of different ages of both sexes using immunoperoxidase labeling with antibodies to bIII-tubulin, tyrosine hydroxylase, syn-aptophysin, PGP9.5, neurofilaments 200kDa, S100, and GFAP. Results. Nerve fibers passing between the lobules, as well as entering them, were positive for bIII-tubulin, tyrosine hydroxylase, PGP9.5 and neurofilaments. Type I cells had cytoplasmic reaction for bIII-tubulin and synaptophysin as well as cytoplasmic and nuclear staining for PGP9.5. At the same time, they had weaker reaction for tyrosine hydroxylase. Type II cells were positive for GFAP and S100. Conclusion. Immunohistochemical characteristics of the human carotid body were similar to those of rats and mice. The human carotid body cells and nerve fibers showed the same distribution of PGP9.5, bIII-tubulin, synaptophysin, neurofilaments, GFAP and S100 as rat and mouse carotid body cells. However, human carotid body reaction for tyrosine hydroxylase was much lower, which may indicate a smaller amount of synthesized catecholamines compared to the carotid body in rats and mice. Keywords: human carotid body, immunohistochemistry, sympathoadrenal system, tyrosine hydroxylase

scholarly journals Immunohistochemical Characteristics of the Human Carotid Body in the Antenatal and Postnatal Periods of Development

2021 ◽  
Vol 22 (15) ◽  
pp. 8222
Author(s):  
Dmitry Otlyga ◽  
Ekaterina Tsvetkova ◽  
Olga Junemann ◽  
Sergey Saveliev
Keyword(s):  
Tyrosine Hydroxylase ◽  
Carotid Body ◽  
Nerve Fibers ◽  
Individual Development ◽  
Endocrine Function ◽  
Type I ◽  
Type I Cells ◽  
Carotid Bodies ◽  
I Cells ◽  
Human Carotid

The evolutionary and ontogenetic development of the carotid body is still understudied. Research aimed at studying the comparative morphology of the organ at different periods in the individual development of various animal species should play a crucial role in understanding the physiology of the carotid body. However, despite more than two centuries of study, the human carotid body remains poorly understood. There are many knowledge gaps in particular related to the antenatal development of this structure. The aim of our work is to study the morphological and immunohistochemical characteristics of the human carotid body in the antenatal and postnatal periods of development. We investigated the human carotid bodies from 1 embryo, 20 fetuses and 13 adults of different ages using samples obtained at autopsy. Immunohistochemistry revealed expression of βIII-tubulin and tyrosine hydroxylase in the type I cells and nerve fibers at all periods of ontogenesis; synaptophysin and PGP9.5 in the type I cells in some of the antenatal cases and all of the postnatal cases; 200 kDa neurofilaments in nerve fibers in some of the antenatal cases and all of the postnatal cases; and GFAP and S100 in the type II cells and Schwann cells in some of the antenatal cases and all of the postnatal cases. A high level of tyrosine hydroxylase in the type I cells was a distinctive feature of the antenatal carotid bodies. On the contrary, in the type I cells of adults, the expression of tyrosine hydroxylase was significantly lower. Our data suggest that the human carotid body may perform an endocrine function in the antenatal period, while in the postnatal period of development, it loses this function and becomes a chemosensory organ.

Characteristics of carotid body chemosensitivity in NADPH oxidase-deficient mice

2002 ◽  
Vol 282 (1) ◽  
pp. C27-C33 ◽  
Author(s):  
L. He ◽  
J. Chen ◽  
B. Dinger ◽  
K. Sanders ◽  
K. Sundar ◽  
...  
Keyword(s):  
Tyrosine Hydroxylase ◽  
Nadph Oxidase ◽  
Carotid Body ◽  
Gene Knockout ◽  
Type I ◽  
Type I Cells ◽  
Carotid Bodies ◽  
Marker Antigen ◽  
I Cells

Various heme-containing proteins have been proposed as primary molecular O2 sensors for hypoxia-sensitive type I cells in the mammalian carotid body. One set of data in particular supports the involvement of a cytochrome b NADPH oxidase that is commonly found in neutrophils. Subunits of this enzyme have been immunocytochemically localized in type I cells, and diphenyleneiodonium, an inhibitor of the oxidase, increases carotid body chemoreceptor activity. The present study evaluated immunocytochemical and functional properties of carotid bodies from normal mice and from mice with a disrupted gp91 phagocytic oxidase (gp91 phox ) DNA sequence gene knockout (KO), a gene that codes for a subunit of the neutrophilic form of NADPH oxidase. Immunostaining for tyrosine hydroxylase, a signature marker antigen for type I cells, was found in groups or lobules of cells displaying morphological features typical of the O2-sensitive cells in other species, and the incidence of tyrosine hydroxylase-immunopositive cells was similar in carotid bodies from both strains of mice. Studies of whole cell K+currents also revealed identical current-voltage relationships and current depression by hypoxia in type I cells dissociated from normal vs. KO animals. Likewise, hypoxia-evoked increases in intracellular Ca2+ concentration were not significantly different for normal and KO type I cells. The whole organ response to hypoxia was evaluated in recordings of carotid sinus nerve activity in vitro. In these experiments, responses elicited by hypoxia and by the classic chemoreceptor stimulant nicotine were also indistinguishable in normal vs. KO preparations. Our data demonstrate that carotid body function remains intact after sequence disruption of the gp91 phox gene. These findings are not in accord with the hypothesis that the phagocytic form of NADPH oxidase acts as a primary O2 sensor in arterial chemoreception.

scholarly journals ULTRASTRUCTURE OF THE CAROTID BODY

1966 ◽  
Vol 30 (3) ◽  
pp. 563-578 ◽  
Author(s):  
T. J. Biscoe ◽  
W. E. Stehbens
Keyword(s):  
Blood Vessels ◽  
Schwann Cells ◽  
Carotid Body ◽  
Nerve Fibers ◽  
Nerve Endings ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Type I Cells ◽  
I Cells

An electron microscope investigation was made of the carotid body in the cat and the rabbit. In thin-walled blood vessels the endothelium was fenestrated. Larger vessels were surrounded by a layer of smooth muscle fibers. Among the numerous blood vessels lay groups of cells of two types covered by basement membranes. Aggregates of Type I cells were invested by Type II cells, though occasionally cytoplasmic extensions were covered by basement membrane only. Type I cells contained many electron-opaque cored vesicles (350 to 1900 A in diameter) resembling those in endocrine secretory cells. Type II cells covered nerve endings terminating on Type I cells and enclosed nerve fibers in much the same manner as Schwann cells. The nerve endings contained numerous microvesicles (∼500 A in diameter), mitochondria, glycogen granules, and a few electron-opaque cored vesicles. Junctions between nerve endings and Type I cells were associated with regions of increased density in both intercellular spaces and the adjoining cytoplasm. Cilia of the 9 + 0 fibril pattern were observed in Type I and Type II cells and pericytes. Nonmyelinated nerve fibers, often containing microvesicles, mitochondria, and a few electron-opaque cored vesicles (650 to 1000 A in diameter) were present in Schwann cells, many of which were situated close to blood vessels Ganglion cells near the periphery of the gland, fibrocytes, and segments of unidentified cells were also seen. It was concluded that, according to present concepts of the structure of nerve endings, those endings related to Type I cells could be efferent or afferent.

Up-regulation of IL-1 receptor type I and tyrosine hydroxylase in the rat carotid body following intraperitoneal injection of IL-1β

2007 ◽  
Vol 128 (6) ◽  
pp. 533-540 ◽  
Author(s):  
Xi-Jing Zhang ◽  
Xi Wang ◽  
Li-Ze Xiong ◽  
Juan Fan ◽  
Xiao-Li Duan ◽  
...  
Keyword(s):  
Tyrosine Hydroxylase ◽  
Carotid Body ◽  
Intraperitoneal Injection ◽  
Receptor Type ◽  
Type I

Autonomic microganglion cells: a source of acetylcholine in the rat carotid body

2004 ◽  
Vol 96 (1) ◽  
pp. 384-391 ◽  
Author(s):  
Estelle B. Gauda ◽  
Reed Cooper ◽  
Shereé M. Johnson ◽  
Gabrielle L. McLemore ◽  
Cathleen Marshall
Keyword(s):  
Carotid Body ◽  
Nerve Fibers ◽  
Hypoxic Exposure ◽  
Type I ◽  
Mrna Levels ◽  
Excitatory Neurotransmitter ◽  
Postnatal Maturation ◽  
Cervical Ganglion ◽  
Cholinergic Nerve Terminals ◽  
Peripheral Arterial

Hypoxic chemosensitivity of peripheral arterial chemoreceptors and the ventilatory response to O2 deprivation increases with postnatal development. Multiple putative neurotransmitters, which are synthesized in the carotid body (CB), are thought to mediate signals generated by hypoxia. Acetylcholine (ACh) is believed to be a major excitatory neurotransmitter participating in hypoxic chemosensitivity. However, it is not known whether ACh originates from type I cells in the CB. In these studies, we tested the hypothesis that choline acetyltransferase (ChAT) and vesicular ACh transporter (VAChT) mRNAs are expressed in the CB and that mRNA levels would increase with postnatal maturation or exposure to hypoxia. Semiquantitative in situ hybridization histochemistry and immunohistochemistry were used to localize cholinergic markers within neurons and cells of the rat CB, the nodose-petrosal-jugular ganglion complex, and the superior cervical ganglion up to postnatal day 28. We show that the pattern of distribution, in tissue sections, is similar for both ACh markers; however, the level of VAChT mRNA is uniformly greater than that of ChAT. VAChT mRNA and immunoreactivity are detected abundantly in the nodose-petrosal-jugular ganglion complex in a number of microganglion cells embedded in nerve fibers innervating the CB for all postnatal groups, whereas ChAT mRNA is detected in only a few of these cells. Contrary to our hypothesis, postnatal maturation caused a reduction in ACh trait expression, whereas hypoxic exposure did not induce the upregulation of VAChT and ChAT mRNA levels in the CB, microganglion, or within the ganglion complex. The present findings indicate that the source of ACh in the CB is likely within autonomic microganglion cells and cholinergic nerve terminals.

Release of Dopamine from Carotid Sinus Nerve Fibers Innervating Type I Cells in the Cat Carotid Body

Neurosignals ◽  
1993 ◽  
Vol 2 (1) ◽  
pp. 16-26 ◽  
Author(s):  
L. Almaraz ◽  
Z.-Z. Wang ◽  
L.J. Stensaas ◽  
S.J. Fidone
Keyword(s):  
Carotid Body ◽  
Carotid Sinus ◽  
Nerve Fibers ◽  
Type I ◽  
Carotid Sinus Nerve ◽  
Type I Cells ◽  
I Cells

Mechanisms of O2 Sensing in the Carotid Body in Comparison With Other O2-Sensing Cells

Physiology ◽  
1995 ◽  
Vol 10 (5) ◽  
pp. 211-216 ◽  
Author(s):  
H Acker ◽  
D Xue
Keyword(s):  
Gene Expression ◽  
Tyrosine Hydroxylase ◽  
Potassium Channel ◽  
Carotid Body ◽  
Type I ◽  
Open Probability ◽  
Signal Cascade ◽  
Sensor Protein ◽  
I Cells ◽  
O2 Sensing

An NAD(P)H oxidase-generating H2O2 dependent on PO2 is proposed as an O2 sensor protein in type I cells of the carotid body, regulating potassium channel open probability as well as tyrosine hydroxylase gene expression. The proposed signal cascade also is important in other O2-sensing cells.

Effect of chronic hypoxia on purinergic synaptic transmission in rat carotid body

2006 ◽  
Vol 100 (1) ◽  
pp. 157-162 ◽  
Author(s):  
L. He ◽  
J. Chen ◽  
B. Dinger ◽  
L. Stensaas ◽  
S. Fidone
Keyword(s):  
Carotid Body ◽  
Chronic Hypoxia ◽  
Cholinergic Receptor ◽  
Nerve Fibers ◽  
Receptor Expression ◽  
Type I ◽  
Simultaneous Exposure ◽  
Type I Cells ◽  
I Cells

Recent studies indicate that chemoafferent nerve fiber excitation in the rat carotid body is mediated by acetylcholine and ATP, acting at nicotinic cholinergic receptors and P2X2 purinoceptors, respectively. We previously demonstrated that, after a 10- to 14-day exposure to chronic hypoxia (CH), the nicotinic cholinergic receptor blocker mecamylamine no longer inhibits rat carotid sinus nerve (CSN) activity evoked by an acute hypoxic challenge. The present experiments examined the effects of CH (9–16 days at 380 Torr) on the expression of P2X2 purinoceptors in carotid body and chemoafferent neurons, as well as the effectiveness of P2X2 receptor blocking drugs on CSN activity evoked by hypoxia. In the normal carotid body, immunocytochemical studies demonstrated a dense plexus of P2X2-positive nerve fibers penetrating lobules of type I cells. In addition, type I cells were lightly stained, indicating P2X2 receptor expression. After CH, the intensity of P2X2 receptor immunostaining was maintained in chemosensory type I cells and in the soma of chemoafferent neurons. P2 receptor expression on type I cells was confirmed by demonstrations of ATP-evoked increased intracellular Ca2+; this response was modulated by simultaneous exposure to hypoxia. In normal preparations, CSN activity evoked by hypoxia in vitro was 65% inhibited in the presence of specific P2X2 receptor antagonists. However, unlike the absence of mecamylamine action after CH, P2X2 antagonists remained effective against hypoxia-evoked activity after CH. Our findings indicate that ATP acting at P2X2 receptors contributes to adjusted chemoreceptor activity after CH, indicating a possible role for purinergic mechanisms in the adaptation of the carotid body in a chronic low-O2 environment.

scholarly journals Characterization of ectonucleotidase expression in the rat carotid body: regulation by chronic hypoxia

2017 ◽  
Vol 313 (3) ◽  
pp. C274-C284 ◽  
Author(s):  
Shaima Salman ◽  
Cathy Vollmer ◽  
Grant B. McClelland ◽  
Colin A. Nurse
Keyword(s):  
Carotid Body ◽  
Chronic Hypoxia ◽  
Purinergic Signaling ◽  
Sensory Nerve ◽  
Nerve Fibers ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Sensory Plasticity ◽  
Cervical Ganglia

The carotid body (CB) chemoreflex maintains blood Po2 and Pco2/H+ homeostasis and displays sensory plasticity during exposure to chronic hypoxia. Purinergic signaling via P1 and P2 receptors plays a pivotal role in shaping the afferent discharge at the sensory synapse containing catecholaminergic chemoreceptor (type I) cells, glial-like type II cells, and sensory (petrosal) nerve endings. However, little is known about the family of ectonucleotidases that control synaptic nucleotide levels. Using quantitative PCR (qPCR), we first compared expression levels of ectonucleoside triphosphate diphosphohydrolases (NTPDases1,2,3,5,6) and ecto-5′-nucleotidase (E5′Nt/CD73) mRNAs in juvenile rat CB vs. brain, petrosal ganglia, sympathetic (superior cervical) ganglia, and a sympathoadrenal chromaffin (MAH) cell line. In whole CB extracts, qPCR revealed a high relative expression of surface-located members NTPDase1,2 and E5′Nt/CD73, compared with low NTPDase3 expression. Immunofluorescence staining of CB sections or dissociated CB cultures localized NTPDase2,3 and E5′Nt/CD73 protein to the periphery of type I clusters, and in association with sensory nerve fibers and/or isolated type II cells. Interestingly, in CBs obtained from rats reared under chronic hypobaric hypoxia (~60 kPa, equivalent to 4,300 m) for 5–7 days, in addition to the expected upregulation of tyrosine hydroxylase and VEGF mRNAs, there was a significant upregulation of NTPDase3 and E5′Nt/CD73 mRNA, but a downregulation of NTPDase1 and NTPDase2 relative to normoxic controls. We conclude that NTPDase1,2,3 and E5′Nt/CD73 are the predominant surface-located ectonucleotidases in the rat CB and suggest that their differential regulation during chronic hypoxia may contribute to CB plasticity via control of synaptic ATP, ADP, and adenosine pools.

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