October 1, 1995The Journal of General PhysiologyOpen Access

Voltage-dependent open-state inactivation of cardiac sodium channels: gating current studies with Anthopleurin-A toxin.

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Population

Single canine cardiac Purkinje cells

Comparison

Anthopleurin-A (Ap-A) toxin vs Control (before modification by Ap-A toxin)

Design

Preclinical

Authors

MSMichael F. SheetsElectrophysiology DHD A HanckNorthwestern University

Discussion

Member takes

Implication

Animal data quantify cardiac Na channel gating charge; leaves open translation to human electrophysiology or antiarrhythmic targets.

Structured PICO

Population

Single canine cardiac Purkinje cells

Intervention

Anthopleurin-A (Ap-A) toxin

Comparator

Control (before modification by Ap-A toxin)

Outcome

Gating charge and voltage dependence of the open state to the inactivated state (O-->I) transitionsurrogate

The study characterizes the voltage dependence and gating charge of the open-to-inactivated state transition in cardiac sodium channels, estimating a valence of 0.75 e- for this transition.

Cite This Study

Sheets et al. (1995) studied this question.

synapsesocial.com/papers/6a70a2fbe36a167817e274d7 https://doi.org/10.1085/jgp.106.4.617

View Full Paper

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Voltage-dependent open-state inactivation of cardiac sodium channels: gating current studies with Anthopleurin-A toxin.

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Voltage-dependent open-state inactivation of cardiac sodium channels: gating current studies with Anthopleurin-A toxin.

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider