Regulation of spontaneous activity and growth of embryonic chick heart cells in tissue culture

1967 ◽  
Vol 16 (3) ◽  
pp. 216-249 ◽  
Author(s):  
Robert L. DeHaan
1950 ◽  
Vol 34 (1) ◽  
pp. 75-79 ◽  
Author(s):  
Wayne Hull ◽  
J. C. Perrone ◽  
Paul L. Kirk

The use of acetyl-3-pyridine and pyridine-3-sulfonic acid as analogues for nicotinic acid has been tested with tissue cultures of embryonic chick heart. Both roller tube and Carrel flask cultures were employed. Cell migration, appearance of the cells, and the uptake of tracer P32 were used as criteria for the action of the analogues. Migration of the cells could be inhibited by both compounds, but at different levels. Both produced abnormal types of cells, but not the same type of abnormality. Uptake of P32 was inhibited by both compounds. Addition of nicotinic acid failed to reverse the effects of the analogues at the concentrations used.


1968 ◽  
Vol 57 (11) ◽  
pp. 1968-1974 ◽  
Author(s):  
W. David Watkins ◽  
Wallace L. Guess

1968 ◽  
Vol 52 (3) ◽  
pp. 643-665 ◽  
Author(s):  
Robert L. DeHaan ◽  
Sheldon H. Gottlieb

Embryonic chick heart cells were cultured on a plastic surface in sparse sheets of 2–50 cells mutually in contact, or isolated as single cells. Conditions are described which permitted conjoint cells to be impaled with recording microelectrodes with 75% success, and isolated single cells with 8% success. It is proposed that cells in electrical contact with neighbors are protected from irreversible damage by the penetrating electrode, by a flow of ions or other substances from connected cells across low-impedance intercellular junctions. Action potentials recorded from conjoint and isolated single cells were similar in form and amplitude. The height or shape of the action potential thus appears not to depend upon spatial relationships of one cell to another. As the external potassium concentration was increased from 1.3 mM to 6 mM, cells became hyperpolarized while the afterhyperpolarization was reduced. At higher potassium levels, the afterhyperpolarization disappeared, the slope of the slow diastolic depolarization decreased, and resting potential fell along a linear curve with a slope of 61 mv per 10-fold increase in potassium. In pacemaker cells the diastolic depolarization consists of two phases: (a) recovery from the afterpotential of the previous action potential and (b) the pacemaker potential. These phases are separated by a point of inflection, and represent manifestations of different mechanisms. Evidence is presented that it is the point of inflection (PBA) rather than the point of maximal diastolic potential, that should be taken as the resting potential.


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