Demonstration of choline acetyltransferase activity in the carotid body of the cat

Ballard, Kathleen J.; Jones, J V

doi:10.1113/jphysiol.1972.sp010021

Cited by 22 publications

(3 citation statements)

References 19 publications

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“…It is worth noting here that these same authors have described the presence of P2Y 1 receptors on type I cells (924). In many ways, this hypothesis has a great number of similarities to earlier ones in which the type II cell was also ascribed a modulatory role in chemotransduction (52, 420, 663), but via type I cell derived ACh rather than ATP. Further studies may be warranted using models in which the type I and type II cells remain in natural contact with each other to establish the true functional role of the type II cell in chemotransduction.…”

Section: Cell Types Of the Carotid Bodymentioning

confidence: 60%

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Kumar

Prabhakar

2012

Comprehensive Physiology

465

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: Cell Types Of the Carotid Bodymentioning

confidence: 60%

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Kumar

Prabhakar

2012

Comprehensive Physiology

465

572

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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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“…Apart from the F.I.F. method, the chromaffine reaction of Hillarp and Hökfelt (in Pearse, 1972) (Kasa et al, 1970) or phospholine jodide (Burt, 1970) iso-Ompa was added to the medium (Ballard & Jones, 1972).…”

Section: Chapter I Introductionmentioning

confidence: 99%