Ultrastructure of the primate carotid body: a morphometric study of the glomus cells and nerve endings in the monkey (Macaca fascicularis)

1985 ◽  
Vol 14 (1) ◽  
pp. 13-32 ◽  
Author(s):  
John T. Hansen
Keyword(s):  
Carotid Body ◽  
Macaca Fascicularis ◽  
Nerve Endings ◽  
Morphometric Study ◽  
Glomus Cells

Transduction mechanisms in carotid body: glomus cells, putative neurotransmitters, and nerve endings

1980 ◽  
Vol 239 (5) ◽  
pp. C135-C152 ◽  
Author(s):  
C. Eyzaguirre ◽  
S. J. Fidone
Keyword(s):  
Carotid Body ◽  
Conclusive Evidence ◽  
Sensory Transduction ◽  
Nerve Endings ◽  
High Pco2 ◽  
Type I ◽  
Glomus Cell ◽  
Impulse Frequency ◽  
Glomus Cells ◽  
Carotid Body Chemoreceptors

Carotid body chemoreceptors are activated by low PO2, high PCO2, acidity, increased temperature, and tonicity. These receptors are important in homeostasis and mediate their reflex effects on the CNS through sensory discharges of the carotid (sinus) nerve. The receptor complex is formed by glomus (type I) cells and carotid nerve endings, which, morphologically, appear to form a sensory synapse. The junction between glomus cells and nerve endings is enveloped by processes of sustentacular (type II) cells. The mechanisms of chemoreceptor transduction are complex; there is no agreement about the identity of the primary receptor element (glomus cell or nerve terminal) or what mechanisms are responsible for the onset of the sensory discharge in the carotid nerve. There is increasing evidence that integrity of the glomus cell is essential for normal transduction and that the receptor synapse described by morphologists may be functionally active. There is no conclusive evidence, however, that the glomus cell is the primary site of sensory transduction. Stimuli act on the glomus cell to release "transmitter" and/or "modulator" substances; but it is unknown if the released chemicals are directly responsible for the accompanying change in sensory impulse frequency or merely modify an already ongoing discharge. Interactions between glomus cells and nerves may be complicated enough to make it very difficult to resolve this question.

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).

Acute O2 sensing through HIF2α-dependent expression of atypical cytochrome oxidase subunits in arterial chemoreceptors

2019 ◽  
Vol 13 (615) ◽  
pp. eaay9452 ◽  
Author(s):  
Alejandro Moreno-Domínguez ◽  
Patricia Ortega-Sáenz ◽  
Lin Gao ◽  
Olalla Colinas ◽  
Paula García-Flores ◽  
...  
Keyword(s):  
Ion Channels ◽  
Carotid Body ◽  
Acute Hypoxia ◽  
Mechanistic Explanation ◽  
Nerve Fibers ◽  
Adaptive Responses ◽  
Glomus Cells ◽  
Adult Mice ◽  
Genes Encoding ◽  
Regulation Of Breathing

Acute cardiorespiratory responses to O2 deficiency are essential for physiological homeostasis. The prototypical acute O2-sensing organ is the carotid body, which contains glomus cells expressing K+ channels whose inhibition by hypoxia leads to transmitter release and activation of nerve fibers terminating in the brainstem respiratory center. The mechanism by which changes in O2 tension modulate ion channels has remained elusive. Glomus cells express genes encoding HIF2α (Epas1) and atypical mitochondrial subunits at high levels, and mitochondrial NADH and reactive oxygen species (ROS) accumulation during hypoxia provides the signal that regulates ion channels. We report that inactivation of Epas1 in adult mice resulted in selective abolition of glomus cell responsiveness to acute hypoxia and the hypoxic ventilatory response. Epas1 deficiency led to the decreased expression of atypical mitochondrial subunits in the carotid body, and genetic deletion of Cox4i2 mimicked the defective hypoxic responses of Epas1-null mice. These findings provide a mechanistic explanation for the acute O2 regulation of breathing, reveal an unanticipated role of HIF2α, and link acute and chronic adaptive responses to hypoxia.

Ultrastructure of sensory nerve endings in monkey (Macaca fascicularis) knee joint capsule

1984 ◽  
Vol 2 (2) ◽  
pp. 169-176 ◽  
Author(s):  
Zdenek Halata ◽  
Marie A. Badalamente ◽  
Roger Dee ◽  
Michael Propper
Keyword(s):  
Knee Joint ◽  
Macaca Fascicularis ◽  
Sensory Nerve ◽  
Joint Capsule ◽  
Nerve Endings ◽  
Sensory Nerve Endings
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