Sodium cyanate-induced opening of calcium-activated potassium currents in hippocampal neuron-derived H19-7 cells

Chin Wei Huang; Chao Ching Huang; Mei Han Huang; Sheng Nan Wu; Yi Jung Hsieh

doi:10.1016/j.neulet.2004.11.081

Sodium cyanate-induced opening of calcium-activated potassium currents in hippocampal neuron-derived H19-7 cells

Chin Wei Huang, Chao Ching Huang, Mei Han Huang, Sheng Nan Wu, Yi Jung Hsieh

Research output: Contribution to journal › Article › peer-review

Abstract

We investigated the chemical toxic agent sodium cyanate (NaOCN) on the large conductance calcium-activated potassium channels (BK_Ca) on hippocampal neuron-derived H19-7 cells. The whole-cell and cell-attach configuration of patch-clamp technique were applied to investigate the BK _Ca currents in H19-7 cells in the presence of NaOCN (0.3 mM). NaOCN activated BK_Ca channels on H19-7 cells. The single-channel conductance of BK_Ca channels was 138 ± 7 pS. The presence of NaOCN (0.3 mM) caused an obvious increase in open probability of BK_Ca channels. NaOCN did not exert effect on the slope of the activation curve and stimulated the activity of BK_Ca channels in a voltage-dependent fashion in H19-7 cells. The presence of paxilline or EGTA significantly reduced the BK_Ca amplitude, in comparison with the presence of NaOCN. These findings suggest that during NaOCN exposure, the activation of BK_Ca channels in neurons could be one of the ionic mechanisms underlying the decreased neuronal excitability and neurological disorders.

Original language	English
Pages (from-to)	110-114
Number of pages	5
Journal	Neuroscience Letters
Volume	377
Issue number	2
DOIs	https://doi.org/10.1016/j.neulet.2004.11.081
Publication status	Published - Mar 29 2005
Externally published	Yes

Keywords

Calcium-activated potassium current
Sodium cyanate

ASJC Scopus subject areas

General Neuroscience

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10.1016/j.neulet.2004.11.081

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title = "Sodium cyanate-induced opening of calcium-activated potassium currents in hippocampal neuron-derived H19-7 cells",

abstract = "We investigated the chemical toxic agent sodium cyanate (NaOCN) on the large conductance calcium-activated potassium channels (BKCa) on hippocampal neuron-derived H19-7 cells. The whole-cell and cell-attach configuration of patch-clamp technique were applied to investigate the BK Ca currents in H19-7 cells in the presence of NaOCN (0.3 mM). NaOCN activated BKCa channels on H19-7 cells. The single-channel conductance of BKCa channels was 138 ± 7 pS. The presence of NaOCN (0.3 mM) caused an obvious increase in open probability of BKCa channels. NaOCN did not exert effect on the slope of the activation curve and stimulated the activity of BKCa channels in a voltage-dependent fashion in H19-7 cells. The presence of paxilline or EGTA significantly reduced the BKCa amplitude, in comparison with the presence of NaOCN. These findings suggest that during NaOCN exposure, the activation of BKCa channels in neurons could be one of the ionic mechanisms underlying the decreased neuronal excitability and neurological disorders.",

keywords = "Calcium-activated potassium current, Sodium cyanate",

author = "Huang, {Chin Wei} and Huang, {Chao Ching} and Huang, {Mei Han} and Wu, {Sheng Nan} and Hsieh, {Yi Jung}",

year = "2005",

month = mar,

day = "29",

doi = "10.1016/j.neulet.2004.11.081",

language = "English",

volume = "377",

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journal = "Neuroscience Letters",

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AU - Huang, Chin Wei

AU - Huang, Chao Ching

AU - Huang, Mei Han

AU - Wu, Sheng Nan

AU - Hsieh, Yi Jung

PY - 2005/3/29

Y1 - 2005/3/29

N2 - We investigated the chemical toxic agent sodium cyanate (NaOCN) on the large conductance calcium-activated potassium channels (BKCa) on hippocampal neuron-derived H19-7 cells. The whole-cell and cell-attach configuration of patch-clamp technique were applied to investigate the BK Ca currents in H19-7 cells in the presence of NaOCN (0.3 mM). NaOCN activated BKCa channels on H19-7 cells. The single-channel conductance of BKCa channels was 138 ± 7 pS. The presence of NaOCN (0.3 mM) caused an obvious increase in open probability of BKCa channels. NaOCN did not exert effect on the slope of the activation curve and stimulated the activity of BKCa channels in a voltage-dependent fashion in H19-7 cells. The presence of paxilline or EGTA significantly reduced the BKCa amplitude, in comparison with the presence of NaOCN. These findings suggest that during NaOCN exposure, the activation of BKCa channels in neurons could be one of the ionic mechanisms underlying the decreased neuronal excitability and neurological disorders.

AB - We investigated the chemical toxic agent sodium cyanate (NaOCN) on the large conductance calcium-activated potassium channels (BKCa) on hippocampal neuron-derived H19-7 cells. The whole-cell and cell-attach configuration of patch-clamp technique were applied to investigate the BK Ca currents in H19-7 cells in the presence of NaOCN (0.3 mM). NaOCN activated BKCa channels on H19-7 cells. The single-channel conductance of BKCa channels was 138 ± 7 pS. The presence of NaOCN (0.3 mM) caused an obvious increase in open probability of BKCa channels. NaOCN did not exert effect on the slope of the activation curve and stimulated the activity of BKCa channels in a voltage-dependent fashion in H19-7 cells. The presence of paxilline or EGTA significantly reduced the BKCa amplitude, in comparison with the presence of NaOCN. These findings suggest that during NaOCN exposure, the activation of BKCa channels in neurons could be one of the ionic mechanisms underlying the decreased neuronal excitability and neurological disorders.

KW - Calcium-activated potassium current

KW - Sodium cyanate

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Sodium cyanate-induced opening of calcium-activated potassium currents in hippocampal neuron-derived H19-7 cells

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Keywords

ASJC Scopus subject areas

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