The main function of the heart is to pump blood to the whole body. To accomplish this task, each individual myocyte in a normal heart needs to be electrically connected and mechanically coordinated with others during a cardiac cycle. The heart is composed of excitable myocytes and nonexcitable cells. The excitable cells are responsible for electrical initiation and conduction to activate the whole heart; they are also responsible for mechanical contraction to pump the blood. Therefore, methods and protocols used for studying cellular electrophysiology of single cardiomyocytes are crucial for understanding physiological functions of a normal heart or pathological mechanisms of a diseased heart. Electrophysiological activity of single cells can be investigated with different techniques either in situ in tissue or in isolated and cultured cells. The classical approach is intracellular recording of electrical activity via inserting a sharp electrode into a cardiomyocyte. However, with the patch clamp technique, scientists have learned more details about molecular structures and functions of ion channels, which are the basis of cardiac electrophysiology. Abnormalities of rhythmic initiation and/or wave conduction along the conductive pathway of a heart can lead to arrhythmias. The methods and techniques used in cellular electrophysiology in recent decades have greatly advanced the knowledge of cardiomyocyte function and arrhythmias at cellular and molecular levels. This chapter describes the patch clamp and other recording methods used for studying cardiac action potentials and ion channels.
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
This is a preview of subscription content, log in to check access.
Neher E, Sakmann B. Single-channel currents recorded from membrane of denervated frog muscle fibres. Nature 1976; 260:799–802.PubMedCrossRefGoogle Scholar
Gussak I, Antzelevitch C, Bjerregaard P, et al. The Brugada syndrome: clinical, electrophysiologic and genetic aspects. J Am Coll Cardiol 1999; 33:5–15.PubMedCrossRefGoogle Scholar
Hille B. Ionic Channels of Excitable Membranes, third edition. Sunderland, MA: Sinauer Associates Inc., 2001.Google Scholar
Hamill OP, Marty A, Neher E, et al. Improved patch clamp techniques for high-resolution current recording from cells and cell-free membrane patches. Pflugers Arch 1981; 391:85–100.PubMedCrossRefGoogle Scholar
Kang JX, Xiao YF, Leaf A. Free, long-chain, polyunsaturated fatty acids reduce membrane electrical excitability in neonatal rat cardiac myocytes. Proc Natl Acad Sci USA 1995; 92:3997–4001.PubMedCrossRefGoogle Scholar
Xiao YF, Kang JX, Morgan JP, et al. Blocking effects of polyunsaturated fatty acids on Na+ channels of neonatal rat ventricular myocytes. Proc Natl Acad Sci USA 1995; 92:11000–4.PubMedCrossRefGoogle Scholar
Xiao YF, Gomez AM, Morgan JP, et al. Suppression of voltage-gated L-type Ca2+ currents by polyunsaturated fatty acids in adult and neonatal rat ventricular myocytes. Proc Natl Acad Sci USA 1997; 94:4182–7.PubMedCrossRefGoogle Scholar
Baruscotti M, Bucchi A, Difrancesco D. Physiology and pharmacology of the cardiac pacemaker (“funny”) current. Pharmacol Ther 2005; 107:59–79.PubMedCrossRefGoogle Scholar
Brown H, Difrancesco D. Voltage-clamp investigations of membrane currents underlying pace-maker activity in rabbit sino-atrial node. J Physiol 1980; 308:331–51.PubMedGoogle Scholar
Stieber J, Hofmann F, Ludwig A. Pacemaker channels and sinus node arrhythmia. Trends Cardiovasc Med 2004; 14:23–8.PubMedCrossRefGoogle Scholar
Dobrzynski H, Boyett MR, Anderson RH. New insights into pacemaker activity: promoting understanding of sick sinus syndrome. Circulation 2007; 115:1921–32.PubMedCrossRefGoogle Scholar
Thollon C, Bedut S, Villeneuve N, et al. Use-dependent inhibition of hHCN4 by ivabradine and relationship with reduction in pacemaker activity. Br J Pharmacol 2007; 150:37–46.PubMedCrossRefGoogle Scholar
Milanesi R, Baruscotti M, Gnecchi-Ruscone T, et al. Familial sinus bradycardia associated with a mutation in the cardiac pacemaker channel. N Engl J Med 2006; 354:151–7.PubMedCrossRefGoogle Scholar
Stieber J, Herrmann S, Feil S, et al. The hyperpolarization-activated channel HCN4 is required for the generation of pacemaker action potentials in the embryonic heart. Proc Natl Acad Sci USA 2003; 100:15235–40.PubMedCrossRefGoogle Scholar
Xiao YF, TenBroek EM, Wilhelm JJ, et al. Electrophysiological characterization of murine HL-5 atrial cardiomyocytes. Am J Physiol Cell Physiol 2006; 291:C407–16.PubMedCrossRefGoogle Scholar
Azene EM, Xue T, Marban E, et al. Non-equilibrium behavior of HCN channels: insights into the role of HCN channels in native and engineered pacemakers. Cardiovasc Res 2005; 67:263–73.PubMedCrossRefGoogle Scholar
Ludwig A, Zong X, Stieber J, et al. Two pacemaker channels from human heart with profoundly different activation kinetics. Embo J 1999; 18:2323–9.PubMedCrossRefGoogle Scholar
Gu Y, Gorelik J, Spohr HA, et al. High-resolution scanning patch clamp: new insights into cell function. Faseb J 2002; 16:748–50.PubMedGoogle Scholar
Gorelik J, Gu Y, Spohr HA, et al. Ion channels in small cells and subcellular structures can be studied with a smart patch clamp system. Biophys J 2002; 83:3296–303.PubMedCrossRefGoogle Scholar