Abstract
The contribution of Ca2+-activated and delayed rectifying K+ channels to the voltage-dependent outward current involved in spike repolarization in mouse pancreatic β-cells (Rorsman, P., and G. Trube. 1986. J. Physiol. 374:531-550) was assessed using patch-clamp techniques. A Ca2+-dependent component could be identified by its rapid inactivation and sensitivity to the Ca2+ channel blocker Cd2+. This current showed the same voltage dependence as the voltage-activated (Cd2+-sensitive) Ca2+ current and contributed 10-20% to the total β-cell delayed outward current. The single-channel events underlying the Ca2+-activated component were investigated in cell-attached patches. Increase of [Ca2+]i invariably induced a dramatic increase in the open state probability of a Ca2+-activated K+ channel. This channel had a single-channel conductance of 70 pS ([K+]o = 5.6 mM). The Ca2+-independent outward current (constituting >80% of the total) reflected the activation of an 8 pS ([K+]o = 5.6 mM; [K+]i = 155 mM) K+ channel. This channel was the only type observed to be associated with action potentials in cell-attached patches. It is suggested that in mouse β-cells spike repolarization results mainly from the opening of the 8-pS delayed rectifying K+ channel.
| Original language | English |
|---|---|
| Pages (from-to) | 1041-1059 |
| Number of pages | 19 |
| Journal | Journal of General Physiology |
| Volume | 95 |
| Issue number | 6 |
| State | Published - Jun 1 1990 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Physiology
Cite this
Delayed rectifying and calcium-activated K+ channels and their significance for action potential repolarization in mouse pancreatic β-cells. / Smith, Paul A.; Bokvist, Krister; Arkhammar, Per; Berggren, Per Olof; Rorsman, Patrik.
In: Journal of General Physiology, Vol. 95, No. 6, 01.06.1990, p. 1041-1059.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Delayed rectifying and calcium-activated K+ channels and their significance for action potential repolarization in mouse pancreatic β-cells
AU - Smith, Paul A.
AU - Bokvist, Krister
AU - Arkhammar, Per
AU - Berggren, Per Olof
AU - Rorsman, Patrik
PY - 1990/6/1
Y1 - 1990/6/1
N2 - The contribution of Ca2+-activated and delayed rectifying K+ channels to the voltage-dependent outward current involved in spike repolarization in mouse pancreatic β-cells (Rorsman, P., and G. Trube. 1986. J. Physiol. 374:531-550) was assessed using patch-clamp techniques. A Ca2+-dependent component could be identified by its rapid inactivation and sensitivity to the Ca2+ channel blocker Cd2+. This current showed the same voltage dependence as the voltage-activated (Cd2+-sensitive) Ca2+ current and contributed 10-20% to the total β-cell delayed outward current. The single-channel events underlying the Ca2+-activated component were investigated in cell-attached patches. Increase of [Ca2+]i invariably induced a dramatic increase in the open state probability of a Ca2+-activated K+ channel. This channel had a single-channel conductance of 70 pS ([K+]o = 5.6 mM). The Ca2+-independent outward current (constituting >80% of the total) reflected the activation of an 8 pS ([K+]o = 5.6 mM; [K+]i = 155 mM) K+ channel. This channel was the only type observed to be associated with action potentials in cell-attached patches. It is suggested that in mouse β-cells spike repolarization results mainly from the opening of the 8-pS delayed rectifying K+ channel.
AB - The contribution of Ca2+-activated and delayed rectifying K+ channels to the voltage-dependent outward current involved in spike repolarization in mouse pancreatic β-cells (Rorsman, P., and G. Trube. 1986. J. Physiol. 374:531-550) was assessed using patch-clamp techniques. A Ca2+-dependent component could be identified by its rapid inactivation and sensitivity to the Ca2+ channel blocker Cd2+. This current showed the same voltage dependence as the voltage-activated (Cd2+-sensitive) Ca2+ current and contributed 10-20% to the total β-cell delayed outward current. The single-channel events underlying the Ca2+-activated component were investigated in cell-attached patches. Increase of [Ca2+]i invariably induced a dramatic increase in the open state probability of a Ca2+-activated K+ channel. This channel had a single-channel conductance of 70 pS ([K+]o = 5.6 mM). The Ca2+-independent outward current (constituting >80% of the total) reflected the activation of an 8 pS ([K+]o = 5.6 mM; [K+]i = 155 mM) K+ channel. This channel was the only type observed to be associated with action potentials in cell-attached patches. It is suggested that in mouse β-cells spike repolarization results mainly from the opening of the 8-pS delayed rectifying K+ channel.
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M3 - Article
C2 - 2197368
AN - SCOPUS:0025309242
VL - 95
SP - 1041
EP - 1059
JO - Journal of General Physiology
JF - Journal of General Physiology
SN - 0022-1295
IS - 6
ER -