Evidence for functional sodium and calcium ion channels in the membrane of cultured cardiomyocytes of the adult rat

1983 ◽  
Vol 61 (11) ◽  
pp. 1312-1316 ◽  
Author(s):  
S. L. Jacobson ◽  
C. B. Kennedy ◽  
G. A. R. Mealing
Keyword(s):  
Action Potentials ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Culture Cells ◽  
Calcium Ion Channels ◽  
Spontaneous Action ◽  
Fetal Bovine ◽  
Spontaneous Action Potentials

Characteristics are reported for electrical activity of adult rat cardiomyocytes in long-term primary culture. Cells in vitro for 12 to 28 days have mean membrane potential of −53 mV, are electrically excitable, and some are spontaneously contractile. The action potential of these cells has a slow rate of depolarization and is abolished by methoxyverapamil (D-600) but not by tetrodotoxin (TTX). When cells are hyperpolarized by passage of an inward current, spontaneous action potentials cease and action potentials evoked by depolarizing pulses are then TTX sensitive. Fetal bovine serum is a constituent of the culture medium. Its temporary removal causes spontaneous contractility to cease but the cells remain electrically excitable.

Electrical properties and synaptic connections to neurons in parasympathetic colonic ganglia of the cat

1984 ◽  
Vol 247 (1) ◽  
pp. G52-G61
Author(s):  
J. Krier ◽  
D. A. Hartman
Keyword(s):  
Synaptic Input ◽  
Action Potentials ◽  
Distal Colon ◽  
Nerve Fibers ◽  
Synaptic Connections ◽  
Electrophysiological Properties ◽  
Intracellular Injection ◽  
Spontaneous Action ◽  
Spontaneous Action Potentials

Intracellular recording techniques were used in vitro to analyze the electrophysiological properties and synaptic connections to cat parasympathetic neurons in ganglia located on the serosal surface of the distal colon. Neurons were classified into two types. The first type exhibited spontaneous action potentials at regular and irregular interspike intervals. Spontaneous action potentials were 1) not abolished by superfusion of the ganglia with a modified Krebs solution containing low Ca2+, high Mg2+, or nicotinic ganglionic blocking agents, 2) reduced or abolished by intracellular injection of hyperpolarizing current, and 3) increased by intracellular injection of depolarizing current. We suggest that the generation of spontaneous action potentials may be due to an endogenous depolarizing mechanism and not to cholinergic synaptic input from other neurons located in the ganglia. The second type of neuron termed "quiescent" exhibited a stable transmembrane potential and elicited action potentials in response to electrical stimulation of nerve trunks. Both quiescent and spontaneously discharging neurons receive synaptic input from preganglionic fibers in the pelvic nerve and project their postganglionic axons to colonic nerve fibers that innervate effector structures in the colon.

scholarly journals Id2 Represses Aldosterone-Stimulated Cardiac T-Type Calcium Channels Expression

2021 ◽  
Vol 22 (7) ◽  
pp. 3561
Author(s):  
Jumpei Ito ◽  
Tomomi Minemura ◽  
Sébastien Wälchli ◽  
Tomoaki Niimi ◽  
Yoshitaka Fujihara ◽  
...  
Keyword(s):  
Transcriptional Repressor ◽  
Neonatal Rat ◽  
Protective Mechanism ◽  
Pathological State ◽  
Rat Cardiomyocytes ◽  
Adult Mice ◽  
Spontaneous Action ◽  
Sirna Knockdown ◽  
Spontaneous Action Potentials ◽  
Ca2 Channels

Aldosterone excess is a cardiovascular risk factor. Aldosterone can directly stimulate an electrical remodeling of cardiomyocytes leading to cardiac arrhythmia and hypertrophy. L-type and T-type voltage-gated calcium (Ca2+) channels expression are increased by aldosterone in cardiomyocytes. To further understand the regulation of these channels expression, we studied the role of a transcriptional repressor, the inhibitor of differentiation/DNA binding protein 2 (Id2). We found that aldosterone inhibited the expression of Id2 in neonatal rat cardiomyocytes and in the heart of adult mice. When Id2 was overexpressed in cardiomyocytes, we observed a reduction in the spontaneous action potentials rate and an arrest in aldosterone-stimulated rate increase. Accordingly, Id2 siRNA knockdown increased this rate. We also observed that CaV1.2 (L-type Ca2+ channel) or CaV3.1, and CaV3.2 (T-type Ca2+ channels) mRNA expression levels and Ca2+ currents were affected by Id2 presence. These observations were further corroborated in a heart specific Id2- transgenic mice. Taken together, our results suggest that Id2 functions as a transcriptional repressor for L- and T-type Ca2+ channels, particularly CaV3.1, in cardiomyocytes and its expression is controlled by aldosterone. We propose that Id2 might contributes to a protective mechanism in cardiomyocytes preventing the presence of channels associated with a pathological state.

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