The fine structural localization of cholinesterases in the carotid body of the cat

Ballard, Kathleen J.; Jones, J V

doi:10.1113/jphysiol.1971.sp009687

Cited by 21 publications

(5 citation statements)

References 24 publications

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“…In support of its role in transmission, however, ACh is found within the carotid body (273, 440) together with choline acetyltransferase, the rate-limiting enzyme for ACh synthesis, in rat (626), cat and rabbit (883), and its degradative enzyme, cholinesterase, (51, 84). The content of ACh has been estimated at 5.6 p mol/carotid body and was little changed following sinus nerve section, which was taken to indicate that ACh was not significantly localized within afferent nerve endings (273) and is most likely stored within the clear vesicles of type I cells.…”

Section: Neurotransmission In the Carotid Bodymentioning

confidence: 99%

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Kumar

Prabhakar

2012

Comprehensive Physiology

453

572

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The discovery of the sensory nature of the carotid body dates back to the beginning of the 20th century. Following these seminal discoveries, research into carotid body mechanisms moved forward progressively through the 20th century, with many descriptions of the ultrastructure of the organ and stimulus-response measurements at the level of the whole organ. The later part of 20th century witnessed the first descriptions of the cellular responses and electrophysiology of isolated and cultured type I and type II cells, and there now exist a number of testable hypotheses of chemotransduction. The goal of this article is to provide a comprehensive review of current concepts on sensory transduction and transmission of the hypoxic stimulus at the carotid body with an emphasis on integrating cellular mechanisms with the whole organ responses and highlighting the gaps or discrepancies in our knowledge. It is increasingly evident that in addition to hypoxia, the carotid body responds to a wide variety of blood-borne stimuli, including reduced glucose and immune-related cytokines and we therefore also consider the evidence for a polymodal function of the carotid body and its implications. It is clear that the sensory function of the carotid body exhibits considerable plasticity in response to the chronic perturbations in environmental O2 that is associated with many physiological and pathological conditions. The mechanisms and consequences of carotid body plasticity in health and disease are discussed in the final sections of this article.

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Section: Neurotransmission In the Carotid Bodymentioning

confidence: 99%

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Kumar

Prabhakar

2012

Comprehensive Physiology

453

572

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“…This article must therefore be hereby marked the occurrence of AcCho (25,) and acetylcholinesterase (32,33) (11) and most probably store NE (39,41).…”

Section: Innervation Of Glomus Cells: Afferent And/or Efferent?mentioning

confidence: 99%

Carotid body chemoreceptor function: hypothesis based on a new circuit model.

Krammer¹

1978

Proc. Natl. Acad. Sci. U.S.A.

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Integration of our own morphological obser- Each component of the carotid bbdy parenchyma has been assumed to be the chemoreceptive one: glomus (type I) cells (1, 3-6), sustentacular (type II) cells (7,8), "free" nerve endings (9), and nerve endings terminating on the type I cells (10, 11). Furthermore, in addition to having a chemoreceptive function, the glomus cells have been considered to be secretory or effector cells (9,(12)(13)(14), interneurons (10, 11), or a combination of these.Perhaps the most generally accepted theory was that glomus cells respond to hypoxia by releasing a neurotransmitter that initiates an increase of firing rate of the nerve fibers terminating on the glomus cells (15). The afferent nature of these fibers was deduced by De Castro (16) from light-microscopic examinations. However, the early ultrastructural studies failed to show evidence of afferent synapses with the glomus cells. On the contrary, these nerve endings were thought to be presynaptic to glomus cells and therefore efferent in function, because they contain large numbers of clear vesicles (17-21). These electron microscopic results were further substantiated by Biscoe et al. (13,22), who reported that nerve endings on glomus cells degenerate after the glossopharyngeal nerve is cut central to the petrosal ganglion. From these results, they concluded that the nerve endings belonged not to afferent axons whose cell bodies were in the petrosal ganglion, but to efferent axons whose cell bodies were in the brain stem. They concluded also that chemoreceptive nerves ended not on glomus cells but elsewhere in the carotid body. These findings and conclusions led to an alternative theory of chemoreceptor function (9)

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“…In the ensuing decades, numerous studies investigated the role of ACh in chemosensation and demonstrated that small quantities of cholinergic agonists and antagonists profoundly altered chemoreceptor discharge 20. Neurochemical investigations indicated that the metabolic machinery necessary for ACh synthesis, storage and inactivation appear to be associated with type I cells in the carotid body 2,3,23,24,31,35,36 and that afferent fibers of the CSN are nearly devoid of cholinergic activity23, 28. In addition, it has been demonstrated that an ACh-like substance is released upon stimulation of the organ in vitrol7, Is.…”

Section: Introductionmentioning

confidence: 99%

Localization and function of cat carotid body nicotinic receptors

et al. 1985

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Key words: acetylcholine --a-bungarotoxin --autoradiography --carotid body --dopamine release --nicotinic receptors Acetylcholine and nicotinic agents excite cat carotid body chemoreceptors and modify their response to natural stimuli. The present experiments utilized [125I]a-bungarotoxin ([125I]a-BGT) to localize within the chemosensory tissue the possible sites of action of exogenous and endogenous nicotinic cholinergic substances. In vitro equilibrium binding studies of intact carotid bodies determined a K d of 5.57 nM and a Bma x of 9.21 pmol/g of tissue. Chronic section (12-15 days) of the carotid sinus nerve (CSN) did not change the amount of displaceable toxin binding. In contrast, the specific binding was reduced by 46% following removal of the superior cervical ganglion. Light microscope autoradiography of normal, CSN-denervated and sympathectomized carotid bodies revealed displaceable binding sites concentrated in lobules of type I and type II cells. Treatment of carotid bodies with 50 nM a-BGT in vitro reduced by 50% the release of [3H]dopamine (synthesized from [3H]tyrosine) caused by hypoxia or nicotine, and also significantly reduced the stimulus-. evoked discharges recorded from the CSN. The data suggest (1) an absence of ct-BGT binding sites on the afferent terminals of the CSN and (2) that nicotinic receptors located within parenchymal cell lobules may modulate the release of catecholamines from these cells.

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The fine structural localization of cholinesterases in the carotid body of the cat

Cited by 21 publications

References 24 publications

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Carotid body chemoreceptor function: hypothesis based on a new circuit model.

Localization and function of cat carotid body nicotinic receptors

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