Rutaecarpine-induced block of delayed rectifier K + current in NG108-15 neuronal cells

Sheng-Nan Wu, Yakking Lo, Hsinyo Chen, Hui Fang Li, Hung Ting Chiang

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34 Citations (Scopus)

Abstract

The effects of rutaecarpine on ionic currents of NG108-15 neuronal cells were investigated in this study. Rutaecarpine (2-100 μM) suppressed the amplitude of delayed rectifier K + current (I K(DR) ) in a concentration-dependent manner. The IC 50 value for rutaecarpine-induced inhibition of I K(DR) was 11 μM. I K(DR) present in these cells is sensitive to the inhibition by quinidine and dendrotoxin, yet not by E-4031. The presence of rutaecarpine enhanced the rate and extent of I K(DR) inactivation, although it had no effect on the initial activation phase of I K(DR) . Recovery from block by rutaecarpine (5 μM) was fitted by a single exponential with a value of 2.87 s. Crossover of tail currents in the presence of rutaecarpine was also observed. Cell-attached single-channel recordings revealed that rutaecarpine decreased channel activity, but it did not alter single-channel amplitude. With the aid of the binding scheme, a quantitative description of the rutaecarpine actions on I K(DR) was provided. However, rutaecarpine (20 μM) had no effect on L-type Ca 2+ current. Under current-clamp configuration, rutaecarpine prolonged action potential duration in NG108-15 cells. These results show that rutaecarpine is a blocker of the K DR channel. The increase in action potential duration induced by rutaecarpine can be explained mainly by its blocking actions on I K(DR) .

Original languageEnglish
Pages (from-to)834-843
Number of pages10
JournalNeuropharmacology
Volume41
Issue number7
DOIs
Publication statusPublished - 2001 Nov 7

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Action Potentials
rutecarpine
Quinidine
E 4031
dendrotoxin

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Cellular and Molecular Neuroscience

Cite this

Wu, Sheng-Nan ; Lo, Yakking ; Chen, Hsinyo ; Li, Hui Fang ; Chiang, Hung Ting. / Rutaecarpine-induced block of delayed rectifier K + current in NG108-15 neuronal cells In: Neuropharmacology. 2001 ; Vol. 41, No. 7. pp. 834-843.
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Rutaecarpine-induced block of delayed rectifier K + current in NG108-15 neuronal cells . / Wu, Sheng-Nan; Lo, Yakking; Chen, Hsinyo; Li, Hui Fang; Chiang, Hung Ting.

In: Neuropharmacology, Vol. 41, No. 7, 07.11.2001, p. 834-843.

Research output: Contribution to journalArticle

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T1 - Rutaecarpine-induced block of delayed rectifier K + current in NG108-15 neuronal cells

AU - Wu, Sheng-Nan

AU - Lo, Yakking

AU - Chen, Hsinyo

AU - Li, Hui Fang

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N2 - The effects of rutaecarpine on ionic currents of NG108-15 neuronal cells were investigated in this study. Rutaecarpine (2-100 μM) suppressed the amplitude of delayed rectifier K + current (I K(DR) ) in a concentration-dependent manner. The IC 50 value for rutaecarpine-induced inhibition of I K(DR) was 11 μM. I K(DR) present in these cells is sensitive to the inhibition by quinidine and dendrotoxin, yet not by E-4031. The presence of rutaecarpine enhanced the rate and extent of I K(DR) inactivation, although it had no effect on the initial activation phase of I K(DR) . Recovery from block by rutaecarpine (5 μM) was fitted by a single exponential with a value of 2.87 s. Crossover of tail currents in the presence of rutaecarpine was also observed. Cell-attached single-channel recordings revealed that rutaecarpine decreased channel activity, but it did not alter single-channel amplitude. With the aid of the binding scheme, a quantitative description of the rutaecarpine actions on I K(DR) was provided. However, rutaecarpine (20 μM) had no effect on L-type Ca 2+ current. Under current-clamp configuration, rutaecarpine prolonged action potential duration in NG108-15 cells. These results show that rutaecarpine is a blocker of the K DR channel. The increase in action potential duration induced by rutaecarpine can be explained mainly by its blocking actions on I K(DR) .

AB - The effects of rutaecarpine on ionic currents of NG108-15 neuronal cells were investigated in this study. Rutaecarpine (2-100 μM) suppressed the amplitude of delayed rectifier K + current (I K(DR) ) in a concentration-dependent manner. The IC 50 value for rutaecarpine-induced inhibition of I K(DR) was 11 μM. I K(DR) present in these cells is sensitive to the inhibition by quinidine and dendrotoxin, yet not by E-4031. The presence of rutaecarpine enhanced the rate and extent of I K(DR) inactivation, although it had no effect on the initial activation phase of I K(DR) . Recovery from block by rutaecarpine (5 μM) was fitted by a single exponential with a value of 2.87 s. Crossover of tail currents in the presence of rutaecarpine was also observed. Cell-attached single-channel recordings revealed that rutaecarpine decreased channel activity, but it did not alter single-channel amplitude. With the aid of the binding scheme, a quantitative description of the rutaecarpine actions on I K(DR) was provided. However, rutaecarpine (20 μM) had no effect on L-type Ca 2+ current. Under current-clamp configuration, rutaecarpine prolonged action potential duration in NG108-15 cells. These results show that rutaecarpine is a blocker of the K DR channel. The increase in action potential duration induced by rutaecarpine can be explained mainly by its blocking actions on I K(DR) .

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