Batrachotoxin protects sodium channels from the blocking action of oenanthotoxin.
1. The blocking action of oenanthotoxin (OETX) and butanol on Na+ channels was studied in voltage clamp experiments on single myelinated nerve fibres treated by batrachotoxin (BTX). 2. OETX (40 microM) blocked Na+ currents through normal channels but did not affect significantly the BTX modified Na+ current. 3. BTX removed the depolarization-induced charge immobilization and slowed down significantly the OFF charge movement. However, the maximum charge displaced, as well as the kinetics of the ON charge movement during a strong membrane depolarization, remained unchanged. 4. OETX blocked the charge movement in normal Na+ channels but did not affect noticeably the charge movement modified by BTX. 5. BTX did not modify the K+ currents and did not protect them from the blocking action of OETX. 6. Butanol (0.01-0.1 M) decreased almost identically and reversibly both normal and BTX-modified Na+ currents. 7. It is concluded that binding of BTX to its receptor protects the Na+ channel from interaction with OETX but left it accessible to butanol.
D020001:1-Butanol; D000480:Alkynes; D000818:Animals; D001496:Batrachotoxins / Q000494:pharmacology*; D000440:Butanols / Q000494:pharmacology; D053281:Enediynes; D005233:Fatty Alcohols / Q000494:pharmacology*; D007473:Ion Channels / Q000187:drug effects*; D011893:Rana esculenta
D000480:Alkynes; D001496:Batrachotoxins; D000440:Butanols; D053281:Enediynes; D005233:Fatty Alcohols; D007473:Ion Channels; C010719:enanthotoxin; D020001:1-Butanol