Na%2b channels in cardiac and neuronal cells derived from a mouse embryonal carcinoma cell line. Article uri icon

abstract

  • 1. Cells from a pluripotent murine embryonal carcinoma cell line (P19) were differentiated in vitro into cells with neurone‐ and cardiac‐like phenotypes. Cells treated with 0.5 microM retinoic acid developed into neurone‐like cells possessing extensive neurites. Dimethyl sulphoxide treatment (0.5%25) produced large, spontaneously contracting cell aggregates with many properties of cardiac cells. 2. The neurone‐ and cardiac‐like cells contained voltage‐sensitive Na%2b channels with properties similar to those of native neuronal and cardiac cells. 3. We used whole‐cell patch clamp techniques to measure inward currents from the neurone‐ and cardiac‐like cells. Undifferentiated (untreated) cells had only small inward currents (peak of ‐0.15 nA in 150 mM external Na%2b). The peak inward current in the neurone‐like and cardiac‐like cells was ‐1.2 nA (in 154 mM external Na%2b) and ‐2.8 nA (in only 46 mM Na%2b), respectively. These large currents were absent when the external solution contained no Na%2b. 4. Tetrodotoxin (TTX) blocked the Na%2b currents in the neurone‐ and cardiac‐like cells in a dose‐dependent manner. The Kd for TTX block of the Na%2b current in the neurone‐like cells was 6.7 nM. The Na%2b current in the cardiac‐like cells was much more resistant to TTX; the half‐blocking concentration was two orders of magnitude higher, 710 nM. 5. The kinetic properties of the Na%2b channel currents in the neurone‐ and cardiac‐like cells were similar but developed over somewhat different voltage ranges. The voltage sensitivity of activation was similar in both cell types but the activation mid‐point voltage was different: ‐12 mV in the neuronal cells and ‐34 mV for cardiac cells. Inactivation of the neuronal Na%2b channels had a mid‐point near ‐47 mV and was more sensitive to the membrane voltage than inactivation of the cardiac channels. The mid‐point of inactivation for the cardiac Na%2b channels was ‐80 mV. © 1993 The Physiological Society

publication date

  • 1993-01-01