Pacemaker Activity of the Pelvicalyceal Border Recorded by an Intracellular Glass Microelectrode

1992 ◽  
Vol 48 (2) ◽  
pp. 121-124 ◽  
Author(s):  
Seigi Tsuchida ◽  
Takashi Suzuki
Keyword(s):  
Pacemaker Activity ◽  
Glass Microelectrode

scholarly journals Effects of Lubiprostone on Pacemaker Activity of Interstitial Cells of Cajal from the Mouse Colon

2014 ◽  
Vol 18 (4) ◽  
pp. 341 ◽  
Author(s):  
Han-Yi Jiao ◽  
Dong Hyun Kim ◽  
Jung Suk Ki ◽  
Kwon Ho Ryu ◽  
Seok Choi ◽  
...  
Keyword(s):  
Interstitial Cells Of Cajal ◽  
Interstitial Cells ◽  
Pacemaker Activity ◽  
Mouse Colon ◽  
Cells Of Cajal

scholarly journals Disease-associated HCN4 V759I variant is not sufficient to impair cardiac pacemaking

2020 ◽  
Vol 472 (12) ◽  
pp. 1733-1742
Author(s):  
Nadine Erlenhardt ◽  
Olaf Kletke ◽  
Franziska Wohlfarth ◽  
Marlene A. Komadowski ◽  
Lukas Clasen ◽  
...  
Keyword(s):  
Family History ◽  
Sick Sinus Syndrome ◽  
Cardiac Pacemaker ◽  
Cell Surface Expression ◽  
Pacemaker Activity ◽  
Hcn Channel ◽  
Functional Interpretation ◽  
Rat Cardiomyocytes ◽  
Cardiac Pacemaking ◽  
History Of

AbstractThe hyperpolarization-activated cation current If is a key determinant for cardiac pacemaker activity. It is conducted by subunits of the hyperpolarization-activated cyclic nucleotide–gated (HCN) channel family, of which HCN4 is predominant in mammalian heart. Both loss-of-function and gain-of-function mutations of the HCN4 gene are associated with sinus node dysfunction in humans; however, their functional impact is not fully understood yet. Here, we sought to characterize a HCN4 V759I variant detected in a patient with a family history of sick sinus syndrome. The genomic analysis yielded a mono-allelic HCN4 V759I variant in a 49-year-old woman presenting with a family history of sick sinus syndrome. This HCN4 variant was previously classified as putatively pathogenic because genetically linked to sudden infant death syndrome and malignant epilepsy. However, detailed electrophysiological and cell biological characterization of HCN4 V759I in Xenopus laevis oocytes and embryonic rat cardiomyocytes, respectively, did not reveal any obvious abnormality. Voltage dependence and kinetics of mutant channel activation, modulation of cAMP-gating by the neuronal HCN channel auxiliary subunit PEX5R, and cell surface expression were indistinguishable from wild-type HCN4. In good agreement, the clinically likewise affected mother of the patient does not exhibit the reported HCN4 variance. HCN4 V759I resembles an innocuous genetic HCN channel variant, which is not sufficient to disturb cardiac pacemaking. Once more, our work emphasizes the importance of careful functional interpretation of genetic findings not only in the context of hereditary cardiac arrhythmias.

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