S. Calvo et al., CATECHOLAMINE SECRETION, CALCIUM LEVELS AND CALCIUM INFLUX IN RESPONSE TO MEMBRANE DEPOLARIZATION IN BOVINE CHROMAFFIN CELLS, Neuroscience, 68(1), 1995, pp. 265-272
In this paper, we show that exposure of chromaffin cells to high K+ (7
5 mM) for 5 min releases about 15% of total norepinephrine and 8% of t
otal epinephrine contained in chromaffin cells. The measured resting m
embrane potential of these cells was -55 mV. Long (10 s) depolarizing
electrical pulses applied from a holding potential of -55 mV to 5 mV,
that would produce a depolarization similar to exposure to high K+ (75
mM), induced an inward Ca2+ current that inactivated with a time cons
tant of about 0.8s and promoted the influx of about 1 fmol of Ca2+ int
o the cell. Both high K+ and electrically-induced depolarization incre
ased intracellular Ca2+ levels to a similar value (about 350 nM). Extr
apolation would indicate that total Ca2+ influx in high K+ (75 mM)-sti
mulated 10(6) chromaffin cells would amount to 1 nmol which would prom
ote the secretion of about 4.9 nmol of norepinephrine and 3.5 nmol of
epinephrine from 10(6) chromaffin cells. The results indicate that Ca2
+ influx in response to depolarization is short-lived, likely due to C
a2+-dependent inactivation of voltage-dependent Ca2+ channels. However
, intracellular Ca2+ levels remain high as long as depolarization is p
resent and long after Ca2+ influx has ceased. This would suggest that
some processes related to either Ca2+ buffering or extrusion from the
cell may be voltage dependent.