Transient and sustained effects of hormones and calcium on membrane potential in a bone cell clone.
Measurements were made of the electrophysiological and cAMP response to changes in extracellular [Ca2+] and to hormone application in a bone cell clone. Both transient and long-term electrophysiological responses were studied. An increase in extracellular [Ca2+] usually resulted in a transient hyperpolarization of about 60-sec duration. In addition, increases in extracellular [Ca2+] from 0.9 to 1.8 mM and from 1.8 to 3.6 mM resulted in long-term hyperpolarization and increased potential fluctuations. Increasing bathing [Ca2+] until the membrane potential reached the K+ equilibrium level resulted in a significant decrease in fluctuations. Addition to the bathing medium of quinine, a putative blocker of the Ca2+-dependent K+ channel, resulted in long-term depolarization of the mean membrane potential, and a long-term decrease in potential fluctuations. Addition of Mg2+, a mild antagonist of Ca2+ entry into the cell, produced transient depolarization and reduction of potential fluctuations. These effects suggest that the potential fluctuations reflect cytoplasmic [Ca2+] fluctuations via Ca2+-dependent K+ membrane channels. Under an extracellular [Ca2+] of 1.8 mM, the application of prostaglandin E2 (PGE2), isoproterenol, and parathyroid hormone produced no significant effect on mean membrane potential or on the sustained potential fluctuations, but PGE2 did significantly raise intracellular cAMP. Under an increased bathing [Ca2+], significant changes in mean potential and fluctuations did occur in response to PGE2, but not in response to the other hormones, while the PGE2 effect on cAMP was not greatly changed. Hyperpolarizing transients of about 30-sec duration occurred in response to all of the hormones, particularly at an extracellular [Ca2+] of 3.6 mM. Thus, there are both transient and long-term electrophysiological responses to hormone application, with only the long-term response correlated with the production of cAMP. These electrophysiological responses may represent separate transient and long-term calcium transport responses to hormone application.
Ferrier
J
J
Illeman
A
A
Zakshek
E
E
D000818:Animals; D001842:Bone and Bones / Q000166:cytology* / Q000187:drug effects; D002118:Calcium / Q000494:pharmacology*; D002460:Cell Line; D002999:Clone Cells; D000242:Cyclic AMP / Q000378:metabolism; D015232:Dinoprostone; D008564:Membrane Potentials / Q000187:drug effects; D008839:Microelectrodes; D010281:Parathyroid Hormone / Q000494:pharmacology*; D011458:Prostaglandins E / Q000494:pharmacology*; D051381:Rats
D010281:Parathyroid Hormone; D011458:Prostaglandins E; D000242:Cyclic AMP; D015232:Dinoprostone; D002118:Calcium