ArticleJournal of biomedical science2009
Developmental expression of a functional TASK-1 2P domain K+ channel in embryonic chick heart.
Article in Journal of biomedical science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 3 citations in OpenAlex.
- Toward the rational design of oncogenic TASK-3 channel inhibitor peptides and nanoconjugate complexes.Frontiers in pharmacology · 2026Review
- The role of acid-sensitive two-pore domain potassium channels in cardiac electrophysiology: focus on arrhythmias.Pflugers Archiv : European journal of physiology · 2015Review
- International Union of Basic and Clinical Pharmacology. LXXIX. Cannabinoid receptors and their ligands: beyond CB₁ and CB₂.Pharmacological reviews · 2010Review
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundBackground K+ channels are the principal determinants of the resting membrane potential (RMP) in cardiac myocytes and thus, influence the magnitude and time course of the action potential (AP).
methodsRT-PCR and in situ hybridization are used to study the distribution of TASK-1 and whole-cell patch clamp technique is employed to determine the functional expression of TASK-1 in embryonic chick heart.
resultsChicken TASK-1 was expressed in the early tubular heart, then substantially decreased in the ventricles by embryonic day 5 (ED5), but remained relatively high in ED5 and ED11 atria. Unlike TASK-1, TASK-3 was uniformly expressed in heart at all developmental stages. In situ hybridization studies further revealed that TASK-1 was expressed throughout myocardium at Hamilton-Hamburger stages 11 and 18 (S11 & S18) heart. In ED11 heart, TASK-1 expression was more restricted to atria. Consistent with TASK-1 expression data, patch clamp studies indicated that there was little TASK-1 current, as measured by the difference currents between pH 8.4 and pH 7.4, in ED5 and ED11 ventricular myocytes. However, TASK-1 current was present in the early embryonic heart and ED11 atrial myocytes. TASK-1 currents were also identified as 3 microM anandamide-sensitive currents. 3 microM anandamide reduced TASK-1 currents by about 58% in ED11 atrial myocytes. Zn2+ (100 microM) which selectively inhibits TASK-3 channel at this concentration had no effect on TASK currents. In ED11 ventricle where TASK-1 expression was down-regulated, IK1 was about 5 times greater than in ED11 atrial myocytes.
conclusionFunctional TASK-1 channels are differentially expressed in the developing chick heart and TASK-1 channels contribute to background K+ conductance in the early tubular embryonic heart and in atria. TASK-1 channels act as a contributor to background K+ current to modulate the cardiac excitability in the embryonic heart that expresses little IK1.
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