Expression of Tandem P Domain K<sup>+</sup>Channel, TREK-1, in the Rat Carotid Body

Yamamoto, Yoshio; Taniguchi, Kazuyuki

doi:10.1369/jhc.5a6755.2005

Cited by 17 publications

(16 citation statements)

References 25 publications

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“…The data in the present study when taken together with reports of Task-2 (Yamamoto et al,, 2002) and Trek-1 (Yamamoto and Taniguchi, 2006), both potassium channels expected to be active at the resting membrane potential, provide a composite description of the channels controlling the resting membrane potential in the terminal fibers. To our knowledge there is only one report of intracellular recording from nerve fibers within the carotid body.…”

Section: Discussionmentioning

confidence: 87%

“…While previous retrograde labeling experiments have identified several voltage-gated K+ (Kv) channel subunits in the soma of petrosal neurons whose axons innervate the carotid body (Andrews and Kunze, 2001), only Kv1.1 (Kline et al, 2005), Task-2 (Yamamoto et al,, 2002), Trek-1 (Yamamoto and Taniguchi, 2006) and Kv1.4 (Sanchez et al 2002) have been identified in nerve terminals in the carotid body. Of particular importance in this chemoreflex pathway is the role of the ion channels which contribute to the resting membrane potential and those channels that, upon depolarization, control discharge patterns of the sensory terminals.…”

Section: Introductionmentioning

confidence: 99%

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Distribution of voltage‐gated potassium and hyperpolarization‐activated channels in sensory afferent fibers in the rat carotid body

Buniel

Glazebrook

Ramirez‐Navarro

et al. 2008

J of Comparative Neurology

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The chemosensory glomus cells of the carotid body (CB) detect changes in O2-tension. Carotid sinus nerve fibers, which originate from peripheral sensory neurons located within the petrosal ganglion, innervate the CB. Release of transmitter from glomus cells activates the sensory afferent fibers to transmit information to the nucleus of the solitary tract in the brainstem. The ion channels expressed within the sensory nerve terminals play an essential role in the ability of the terminal to initiate action potentials in response to transmitter-evoked depolarization. However, with a few exceptions, the identity of ion channels expressed in these peripheral nerve fibers is unknown. This study addresses the expression of voltage-gated channels in the sensory fibers with a focus on channels that set the resting membrane potential and regulate discharge patterns. Using immunohistochemistry and fluorescence confocal microscopy, potassium channel subunits and HCN (hyperpolarization-activated) family members were localized both in petrosal neurons that expressed tyrosine hydroxylase, and the CSN axons within the carotid body. Channels contributing to resting membrane potential including HCN2, responsible in part for Ih current, and the KCNQ2 and KCNQ5 subunits thought to underlie the neuronal “M current” were identified in the sensory neurons and their axons innervating the carotid body. In addition, the results presented here demonstrate expression of several potassium channels that shape the action potential and the frequency of discharge including Kv1.4, Kv1.5, Kv4.3, KCa (BK). The role of these channels should be considered in interpretation of the fiber discharge in response to perturbation of the carotid body environment.

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Section: Discussionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Distribution of voltage‐gated potassium and hyperpolarization‐activated channels in sensory afferent fibers in the rat carotid body

Buniel

Glazebrook

Ramirez‐Navarro

et al. 2008

J of Comparative Neurology

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“…Additional support for an action of AMPK on O 2 -sensitive currents, comes from HEK293 cells, where AICAR was shown to significantly inhibit outward current via heterologously expressed, rodent TWIK-related K + channel, TREK-1 (KCNK2) and TREK-2 (KCNK10), background K + channels (468), that have been identified in type I cells (929). Hypoxia (11 mmHg Po 2 ; 6–7 min) could also, reversibly, inhibit TREK conductance by around 40%.…”

Section: Sensing Hypoxia—transduction Processes In the Carotid Bodymentioning

confidence: 99%

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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“…Although rat carotid body type 1 cells are reported to express TASK-1 mRNA [19], TREK-1 mRNA [207], and TASK-2-, TASK-3-, and TRAAK-like immunoreactivity [206], the properties of the oxygen-sensitive leak K + channel appeared most similar to TASK-1 [19,203]. The oxygen-sensitive component of the macroscopic leak current was inhibited by more than 50% in response to lowering extracellular pH to 6.4, stimulated by halothane, and weakly sensitive to Zn 2+ (50% inhibition at 200 lM) (see Table 4).…”

Section: Oxygen Sensitivitymentioning

confidence: 99%

Biophysical, pharmacological, and functional characteristics of cloned and native mammalian two-pore domain K+ channels

Lotshaw

2007

Cell Biochem Biophys

166

185

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The mammalian family of two-pore domain K+ (K2P) channel proteins are encoded by 15 KCNK genes and subdivided into six subfamilies on the basis of sequence similarities: TWIK, TREK, TASK, TALK, THIK, and TRESK. K2P channels are expressed in cells throughout the body and have been implicated in diverse cellular functions including maintenance of the resting potential and regulation of excitability, sensory transduction, ion transport, and cell volume regulation, as well as metabolic regulation and apoptosis. In recent years K2P channel isoforms have been identified as important targets of several widely employed drugs, including: general anesthetics, local anesthetics, neuroprotectants, and anti-depressants. An important goal of future studies will be to identify the basis of drug actions and channel isoform selectivity. This goal will be facilitated by characterization of native K2P channel isoforms, their pharmacological properties and tissue-specific expression patterns. To this end the present review examines the biophysical, pharmacological, and functional characteristics of cloned mammalian K2P channels and compares this information with the limited data available for native K2P channels in order to determine criteria which may be useful in identifying ionic currents mediated by native channel isoforms and investigating their pharmacological and functional characteristics.

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Expression of Tandem P Domain K⁺Channel, TREK-1, in the Rat Carotid Body

Cited by 17 publications

References 25 publications

Distribution of voltage‐gated potassium and hyperpolarization‐activated channels in sensory afferent fibers in the rat carotid body

Distribution of voltage‐gated potassium and hyperpolarization‐activated channels in sensory afferent fibers in the rat carotid body

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Biophysical, pharmacological, and functional characteristics of cloned and native mammalian two-pore domain K+ channels

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Expression of Tandem P Domain K+Channel, TREK-1, in the Rat Carotid Body

Cited by 17 publications

References 25 publications

Distribution of voltage‐gated potassium and hyperpolarization‐activated channels in sensory afferent fibers in the rat carotid body

Distribution of voltage‐gated potassium and hyperpolarization‐activated channels in sensory afferent fibers in the rat carotid body

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Biophysical, pharmacological, and functional characteristics of cloned and native mammalian two-pore domain K+ channels

Contact Info

Product

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Expression of Tandem P Domain K⁺Channel, TREK-1, in the Rat Carotid Body