1983
DOI: 10.2170/jjphysiol.33.777
|View full text |Cite
|
Sign up to set email alerts
|

Prolonged action potential of frog skeletal muscle membrane in Ca-free EGTA solution.

Abstract: The membrane of isolated frog skeletal muscle fibers with or without T-system is depolarized to about -30 mV in a Ca-free solution containing 2 mM EGTA. Under such a condition, the action potential can be produced by a cathodal pulse when the membrane is previously hyperpolarized to -70--100 mV by a conditioning anodal current. The action potential consists of two different potential components, namely a spike potential and a following slow depolarizing response forming a plateau phase (plateau potential). The… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1

Citation Types

0
1
0

Year Published

1986
1986
1992
1992

Publication Types

Select...
5

Relationship

0
5

Authors

Journals

citations
Cited by 5 publications
(1 citation statement)
references
References 25 publications
(30 reference statements)
0
1
0
Order By: Relevance
“…Sodium entry must also be through calcium channels, which are known to lose their specificity under low calcium conditions (Tunstall et al, 1986) since cadmium and nickel, two well-described calcium channel blockers (Frank et al, 1982;Rich and Langer, 1982), prevent the paradoxical increase as well. The depolarization caused by low external calcium (Almers et al, 1984;Minota and Koketsu, 1983) and intracellular sodium loading by either means are, however, apparently able to shift the exchanger into its reverse phase when it is reactivated by external calcium during reperfusion (Caputo et al, 1989;DiPolo and Beauge, 1988).…”
Section: Sodium Entry As a Precursor To Calcium Paradoxmentioning
confidence: 99%
“…Sodium entry must also be through calcium channels, which are known to lose their specificity under low calcium conditions (Tunstall et al, 1986) since cadmium and nickel, two well-described calcium channel blockers (Frank et al, 1982;Rich and Langer, 1982), prevent the paradoxical increase as well. The depolarization caused by low external calcium (Almers et al, 1984;Minota and Koketsu, 1983) and intracellular sodium loading by either means are, however, apparently able to shift the exchanger into its reverse phase when it is reactivated by external calcium during reperfusion (Caputo et al, 1989;DiPolo and Beauge, 1988).…”
Section: Sodium Entry As a Precursor To Calcium Paradoxmentioning
confidence: 99%