AdE-1, a cardiotonic peptide recently isolated from the sea anemone Aiptasia diaphana, contains 44 amino acids and has a molecular mass of 4907 Da. It was previously found to resemble other sea anemone type 1 and 2 Na+ channel toxins, enhancing contractions of rat cardiomyocytes and slowing their twitch relaxation; however, it did not induce spontaneous twitches. AdE-1 increased the duration of the cardiomyocyte action potential and decreased its amplitude and its time-to-peak in a concentration-dependent manner, without affecting its threshold and cell resting potential. Nor did it generate the early and delayed after-depolarizations characteristic of sea anemone Na+ channel toxins. To further understand its mechanism of action we investigated the effect of AdE-1 on the major ion currents of rat cardiomyocytes. In the present study we show that AdE-1 markedly slowed inactivation of the Na+ current, enhancing and prolonging the current influx with no effect on current activation, possibly through direct interaction with the site 3 receptor of the Na+ channel. No significant effect of AdE-1 on the Ca2+ current was observed, but, unexpectedly, AdE-1 significantly increased the amplitude of the transient component of the K+ current, shifting the current threshold to more negative membrane potentials. This effect on the K+ current has not been found in any other sea anemone toxin and may explain the exclusive reduction in action potential amplitude and the absence of the action potential disorders found with other toxins, such as early and delayed after-depolarizations.
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Research Article|
June 13 2014
The sea anemone toxin AdE-1 modifies both sodium and potassium currents of rat cardiomyocytes
Nir Nesher;
Nir Nesher
1
*Department of Cell and Animal Biology, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
†Department of Neurobiology, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
1To whom correspondence should be addressed (email nir.nesher@mail.huji.ac.il).
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Eliahu Zlotkin;
Eliahu Zlotkin
2
*Department of Cell and Animal Biology, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
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Binyamin Hochner
Binyamin Hochner
†Department of Neurobiology, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
‡The Interdisciplinary Center for Neuronal Computation, Institute of Life Sciences, Hebrew University of Jerusalem, Jerusalem, Israel
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Publisher: Portland Press Ltd
Received:
November 05 2013
Revision Received:
March 28 2014
Accepted:
April 22 2014
Accepted Manuscript online:
April 22 2014
Online ISSN: 1470-8728
Print ISSN: 0264-6021
© The Authors Journal compilation © 2014 Biochemical Society
2014
Biochem J (2014) 461 (1): 51–59.
Article history
Received:
November 05 2013
Revision Received:
March 28 2014
Accepted:
April 22 2014
Accepted Manuscript online:
April 22 2014
Citation
Nir Nesher, Eliahu Zlotkin, Binyamin Hochner; The sea anemone toxin AdE-1 modifies both sodium and potassium currents of rat cardiomyocytes. Biochem J 1 July 2014; 461 (1): 51–59. doi: https://doi.org/10.1042/BJ20131454
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