Abstract
Tedisamil, a bradycardic compound in heart, also acts on K + channels in neurons. We determined the actions of tedisamil on action potentials in CA1 pyramidal neurons in hippocampal slices and on BK-type Ca 2+-activated K + channel activity in inside-out patches excised from hippocampal neurons. In slices, tedisamil (5 μM) attenuated the fast afterhyperpolarization (AHP) and prolonged the repolarization phase of the action potential. Additionally, the compound induced burst-firing activity and enhanced the slow AHP that follows a train of action potentials. The single channel data showed tedisamil actions to be consistent with open channel blockade of the BK-type of K + channel. Together, the results are consistent with the possibility that prolongation of the action potential by tedisamil is mediated by a tetraethylammonium-like effect of the agent to block BK-type Ca 2+-activated K + channels. The study also points to a number of effects that may contribute to the known nervous system toxicity induced by tedisamil.
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