Wg. Ding et al., A POSSIBLE ROLE OF THE ATP-SENSITIVE POTASSIUM-ION CHANNEL IN DETERMINING THE DURATION OF SPIKE-BURSTS IN MOUSE PANCREATIC BETA-CELLS, Biochimica et biophysica acta. Biomembranes, 1279(2), 1996, pp. 219-226
The pancreatic beta-cell displays an electrical activity consisting of
spike bursts and silent phases at glucose concentrations of about 10
mM. The mechanism of initial depolarization induced by glucose is well
defined. However, the mechanism inducing the silent phase has not bee
n fully elucidated. In the present study, the possibility of involveme
nt of ATP-sensitive K+ channels in repolarization was examined using t
he patch-clamp technique in the cell-attached recording configuration.
Ouabain (0.1 mM), an inhibitor of Na+/K+-ATPase, caused a complete: s
uppression of ATP-sensitive K+ channel activity followed by typical bi
phasic current deflections, which were due to action potentials. The c
hannel activity was also inhibited by removal of K+ from a perifusion
solution. Furthermore, the activity of ATP-sensitive K+ channels was m
arkedly inhibited either by replacement of external NaCl with LiCl or
by addition of amiloride (0.2 mM), a blocker of Na+/H+ antiport. Addit
ion of L-type Ca2+ channel blockers such as Nifedipine or Mn2+ induced
the complete suppression of K+ channel activity, These findings stron
gly suggest that a fall in ATP consumption results in sustained depola
rization, and that the repolarizations interposed between spike-bursts
under normal ionic conditions are due to the periodical fall of ATP c
oncentration brought about by periodical acceleration of ATP consumpti
on at Na+/K+-pumps. It is concluded that the elevation of intracellula
r Na+ concentration as a consequence of accelerated Na+/Ca2+-countertr
ansport during the period of spike-burst enhances ATP consumption, lea
ding to a fall in ATP concentration which is responsible for terminati
on of spike-burst and initiation of repolarization.