The TASK Family: Two-Pore Domain Background K+ Channels

Bayliss, Douglas A.; Sirois, Jay E.; Talley, Edmund M.

doi:10.1124/mi.3.4.205

Cited by 127 publications

(138 citation statements)

References 80 publications

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“…These data indicate that zone-specific expression of CYP11␤1 and CYP11␤2 was unaltered in TASK Ϫ/Ϫ mice; they provide added indication that there are no overt abnormalities in adrenal gland structure that arise from TASK channel deletion, and they support the use of our conventional TASK knockout lines in the proposed studies. Interestingly, a recent study reports sex differences in effects of TASK-1 subunit deletion on adrenal development and zonation; males appear normal, and females show marked developmental abnormalities (25). Our data extend these observations showing that adrenals from male mice lacking both TASK-1 and TASK-3 are also normal in morphology and zonation.…”

Section: Resultssupporting

confidence: 80%

“…1C, Upper Left). By contrast, TASK-3 transcripts were localized primarily to the outer ZG and the inner zona medullaris and were absent from the zona fasciculata (25) (Fig. 1C, Lower Left); as expected, neither TASK-1 nor TASK-3 mRNA was expressed in adrenal glands of TASK Ϫ/Ϫ mice (Fig.…”

Section: Resultsmentioning

confidence: 95%

“…www.pnas.org͞cgi͞doi͞10.1073͞pnas.0807088105 PHYSIOLOGY. For the article ''TASK channel deletion in mice causes primary hyperaldosteronism,'' by Lucinda A. Davies, Changlong Hu, Nick A. Guagliardo, Neil Sen, Xiangdong Chen, Edmund M. Talley, Robert M. Carey, Douglas A. Bayliss, and Paula Q. Barrett, which appeared in issue 6, February 12, 2008, of Proc Natl Acad Sci USA (105:2203-2208; first published February 4, 2008;10.1073͞pnas.0712000105), the authors note that on page 2204, right column, line 18, the statement ''a recent study reports sex differences in effects of TASK-1 subunit deletion on adrenal development and zonation; males appear normal, and females show marked developmental abnormalities (25)'' is misreferenced and should instead cite ref. 48.…”

mentioning

confidence: 99%

“…These channels show little or no voltage dependence and only mild rectification properties in physiological asymmetric K solutions. By generating leak or background K currents, they play a principal role in setting negative membrane voltages (24,25). TASK-1 and TASK-3 channels are inhibited by extracellular protons in the physiological range and by hormones that activate G q -coupled receptors (26).…”

mentioning

confidence: 99%

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TASK channel deletion in mice causes primary hyperaldosteronism

Davies¹,

Hu²,

Guagliardo³

et al. 2008

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

171

166

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When inappropriate for salt status, the mineralocorticoid aldosterone induces cardiac and renal injury. Autonomous overproduction of aldosterone from the adrenal zona glomerulosa (ZG) is also the most frequent cause of secondary hypertension. Yet, the etiology of nontumorigenic primary hyperaldosteronism caused by bilateral idiopathic hyperaldosteronism remains unknown. Here, we show that genetic deletion of TWIK-related acid-sensitive K (TASK)-1 and TASK-3 channels removes an important background K current that results in a marked depolarization of ZG cell membrane potential. Although TASK channel deletion mice (TASK −/− ) adjust urinary Na excretion and aldosterone production to match Na intake, they produce more aldosterone than control mice across the range of Na intake. Overproduction of aldosterone is not the result of enhanced activity of the renin–angiotensin system because circulating renin concentrations remain either unchanged or lower than those of control mice at each level of Na intake. In addition, TASK −/− mice fail to suppress aldosterone production in response to dietary Na loading. Autonomous aldosterone production is also demonstrated by the failure of an angiotensin type 1 receptor blocker, candesartan, to normalize aldosterone production to control levels in TASK −/− mice. Thus, TASK −/− channel knockout mice exhibit the hallmarks of primary hyperaldosteronism. Our studies establish an animal model of nontumorigenic primary hyperaldosteronism and identify TASK channels as a possible therapeutic target for primary hyperaldosteronism.

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Section: Resultssupporting

confidence: 80%

Section: Resultsmentioning

confidence: 95%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

TASK channel deletion in mice causes primary hyperaldosteronism

Davies¹,

Hu²,

Guagliardo³

et al. 2008

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

171

166

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“…Thus, Leak is a major determinant of preMN/MN excitability. TASK channels contribute to Leak at least in XII MNs (Talley et al, 2000;Bayliss et al, 2003); modulation of Leak via these channels (Talley et al, 2000) may provide a fundamental mechanism for excitability control.…”

Section: Functional Significance Of Nap and Leak In Premns And Mnsmentioning

confidence: 99%

Functional Imaging, Spatial Reconstruction, and Biophysical Analysis of a Respiratory Motor Circuit IsolatedIn Vitro

Wilson²,

et al. 2008

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We combined real-time calcium-based neural activity imaging with whole-cell patch-clamp recording techniques to map the spatial organization and analyze electrophysiological properties of respiratory neurons forming the circuit transmitting rhythmic drive from the pre-Bötzinger complex (pre-BötC) through premotoneurons to hypoglossal (XII) motoneurons. Inspiratory pre-BötC neurons, XII premotoneurons (preMNs), and XII motoneurons (MNs) were retrogradely labeled with Ca 2ϩ -sensitive dye in neonatal rat in vitro brainstem slices. PreMN cell bodies were arrayed dorsomedially to pre-BötC neurons with little spatial overlap; axonal projections to MNs were ipsilateral. Inspiratory MNs were distributed in dorsal and ventral subnuclei of XII. Voltage-clamp recordings revealed that two currents, persistent sodium current (NaP) and K ϩ -dominated leak current (Leak), primarily contribute to preMN/MN subthreshold current-voltage relationships. NaP or Leak conductance densities in preMNs and MNs were not significantly different. We quantified preMN and MN action potential time course and spike frequency-current ( f-I) relationships and found no significant differences in repetitive spiking dynamics, steady-state f-I gains, and afterpolarizing potentials. Rhythmic synaptic drive current densities were similar in preMNs and MNs. Our results indicate that, despite topographic and morphological differences, preMNs and MNs have some common intrinsic membrane, synaptic integration, and spiking properties that we postulate ensure fidelity of inspiratory drive transmission and conversion of synaptic drive into (pre)motor output. There also appears to be a common architectonic organization for some respiratory drive transmission circuits whereby many preMNs are spatially segregated from pre-BötC rhythm-generating neurons, which we hypothesize may facilitate downstream integration of convergent inputs for premotor pattern formation.

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Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Kumar

Prabhakar

2012

Comprehensive Physiology

449

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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The TASK Family: Two-Pore Domain Background K+ Channels

Cited by 127 publications

References 80 publications

TASK channel deletion in mice causes primary hyperaldosteronism

TASK channel deletion in mice causes primary hyperaldosteronism

Functional Imaging, Spatial Reconstruction, and Biophysical Analysis of a Respiratory Motor Circuit IsolatedIn Vitro

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

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