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Selected Publication:
Schreibmayer, W; Kazerani, H; Tritthart, HA.
A mechanistic interpretation of the action of toxin II from Anemonia sulcata on the cardiac sodium channel.
Biochim Biophys Acta. 1987; 901(2):273-282
Doi: 10.1016/0005-2736(87)90124-6
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- Leading authors Med Uni Graz
- Schreibmayer Wolfgang
- Co-authors Med Uni Graz
- Tritthart Helmut
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- Abstract:
- Cardiac sodium channels, modified by Anemonia sulcata toxin II, have been analyzed by the patch-clamp method. The open state of the modified sodium channels proved to be prolonged highly significantly and reopening from a closed state denoted c*-state frequently occurred, interrupted by silent periods, denoted i*-state. Activation from the c*-state was apparently not affected by toxin action, whereas activation from the i*-state was markedly prolonged. Upon higher depolarizations toxin-induced sodium channels disappeared and this behaviour has been attributed to dissociation of the toxin from the channel by use of a special pulse-protocol. The onset of the toxin effect on the action potential proved to depend on stimulation, and it is concluded that the toxin binds preferentially to the open (o)-state. Taking together the results, a kinetic scheme is suggested for action of the toxin on the cardiac sodium channel.
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