Abstract
A prolonged hyperpolarizing afterpotential (amplitude 5-20 mV, half decay time about 400 msec at 25°C) follows the action potential in myotubes and myosacs cultured from rat skeletal muscle. This slow hyperpolarizing afterpotential (hap) is mediated by an increase in membrane K conductance, because its reversal potential follows the Nernst potential for K and is not affected by other ions. The conductance increase measured during the hap (up to four times the resting input conductance) correctly predicts the time course of the slow hap. The slow hap is Ca dependent. Its amplitude decreases when bath [Ca] is lowered, and both amplitude and duration increase when bath [Ca] is raised. The slow hap is blocked by intracellular injection of the calcium chelator, EGTA. It is inhibited by solutions containing 2-4 mM manganese or 1-5 mM barium, but is not blocked by 5-20 mM tetraethylammonium. Myotubes bathed in zero [Na], high [Ca] solutions show calcium action potentials, which are inhibited by 2-10 mM manganese, nickel or cobalt. Myotubes bathed in isotonic Ca salts (or in 2 mM Ca plus 5 mM caffeine) show long-lasting (up to 10 sec) spontaneous hyperpolarizations accompanied by prolonged contractions. These hyperpolarizations are associated with a large increase in input conductance, and they reverse in sign near the K equilibrium potential. They appear to reflect activation of the Ca-sensitive K conductance by Ca released from intracellular stores. The observation that spontaneous hyperpolarizations usually occur with no prior depolarization argues that at least a portion of the slow, Ca-sensitive K conductance system can be activated by internal Ca alone, with no requirement for plasma membrane depolarization. Cultured myotubes also have a faster K conductance system, which is inhibited by 5-20 mM tetraethylammonium or 1-5 mM barium, and is not dependent on Ca for its activation.
| Original language | English |
|---|---|
| Pages (from-to) | 258-266 |
| Number of pages | 9 |
| Journal | Developmental Biology |
| Volume | 82 |
| Issue number | 2 |
| DOIs | |
| State | Published - Jan 1 1981 |
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Calcium-dependent slow potassium conductance in rat skeletal myotubes. / Barrett, John; Barrett, Ellen; Dribin, Lori B.
In: Developmental Biology, Vol. 82, No. 2, 01.01.1981, p. 258-266.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Calcium-dependent slow potassium conductance in rat skeletal myotubes
AU - Barrett, John
AU - Barrett, Ellen
AU - Dribin, Lori B.
PY - 1981/1/1
Y1 - 1981/1/1
N2 - A prolonged hyperpolarizing afterpotential (amplitude 5-20 mV, half decay time about 400 msec at 25°C) follows the action potential in myotubes and myosacs cultured from rat skeletal muscle. This slow hyperpolarizing afterpotential (hap) is mediated by an increase in membrane K conductance, because its reversal potential follows the Nernst potential for K and is not affected by other ions. The conductance increase measured during the hap (up to four times the resting input conductance) correctly predicts the time course of the slow hap. The slow hap is Ca dependent. Its amplitude decreases when bath [Ca] is lowered, and both amplitude and duration increase when bath [Ca] is raised. The slow hap is blocked by intracellular injection of the calcium chelator, EGTA. It is inhibited by solutions containing 2-4 mM manganese or 1-5 mM barium, but is not blocked by 5-20 mM tetraethylammonium. Myotubes bathed in zero [Na], high [Ca] solutions show calcium action potentials, which are inhibited by 2-10 mM manganese, nickel or cobalt. Myotubes bathed in isotonic Ca salts (or in 2 mM Ca plus 5 mM caffeine) show long-lasting (up to 10 sec) spontaneous hyperpolarizations accompanied by prolonged contractions. These hyperpolarizations are associated with a large increase in input conductance, and they reverse in sign near the K equilibrium potential. They appear to reflect activation of the Ca-sensitive K conductance by Ca released from intracellular stores. The observation that spontaneous hyperpolarizations usually occur with no prior depolarization argues that at least a portion of the slow, Ca-sensitive K conductance system can be activated by internal Ca alone, with no requirement for plasma membrane depolarization. Cultured myotubes also have a faster K conductance system, which is inhibited by 5-20 mM tetraethylammonium or 1-5 mM barium, and is not dependent on Ca for its activation.
AB - A prolonged hyperpolarizing afterpotential (amplitude 5-20 mV, half decay time about 400 msec at 25°C) follows the action potential in myotubes and myosacs cultured from rat skeletal muscle. This slow hyperpolarizing afterpotential (hap) is mediated by an increase in membrane K conductance, because its reversal potential follows the Nernst potential for K and is not affected by other ions. The conductance increase measured during the hap (up to four times the resting input conductance) correctly predicts the time course of the slow hap. The slow hap is Ca dependent. Its amplitude decreases when bath [Ca] is lowered, and both amplitude and duration increase when bath [Ca] is raised. The slow hap is blocked by intracellular injection of the calcium chelator, EGTA. It is inhibited by solutions containing 2-4 mM manganese or 1-5 mM barium, but is not blocked by 5-20 mM tetraethylammonium. Myotubes bathed in zero [Na], high [Ca] solutions show calcium action potentials, which are inhibited by 2-10 mM manganese, nickel or cobalt. Myotubes bathed in isotonic Ca salts (or in 2 mM Ca plus 5 mM caffeine) show long-lasting (up to 10 sec) spontaneous hyperpolarizations accompanied by prolonged contractions. These hyperpolarizations are associated with a large increase in input conductance, and they reverse in sign near the K equilibrium potential. They appear to reflect activation of the Ca-sensitive K conductance by Ca released from intracellular stores. The observation that spontaneous hyperpolarizations usually occur with no prior depolarization argues that at least a portion of the slow, Ca-sensitive K conductance system can be activated by internal Ca alone, with no requirement for plasma membrane depolarization. Cultured myotubes also have a faster K conductance system, which is inhibited by 5-20 mM tetraethylammonium or 1-5 mM barium, and is not dependent on Ca for its activation.
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UR - http://www.scopus.com/inward/citedby.url?scp=0019524260&partnerID=8YFLogxK
U2 - 10.1016/0012-1606(81)90450-4
DO - 10.1016/0012-1606(81)90450-4
M3 - Article
C2 - 7227642
AN - SCOPUS:0019524260
VL - 82
SP - 258
EP - 266
JO - Developmental Biology
JF - Developmental Biology
SN - 0012-1606
IS - 2
ER -