Sodium cyanate-induced opening of calcium-activated potassium currents in hippocampal neuron-derived H19-7 cells.
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+/-7pS. 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.
Huang
Chin-Wei
CW
Department of Neurology, National Cheng-Kung University Medical Center, No. 1, University Road, Tainan, Taiwan.
Huang
Chao-Ching
CC
Huang
Mei-Han
MH
Wu
Sheng-Nan
SN
Hsieh
Yi-Jung
YJ
D000818:Animals; D002460:Cell Line; D003485:Cyanates / Q000494:pharmacology*; D006624:Hippocampus / Q000187:drug effects* / Q000502:physiology; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D024681:Potassium Channels, Calcium-Activated / Q000819:agonists / Q000502:physiology*; D051381:Rats
D003485:Cyanates; D024681:Potassium Channels, Calcium-Activated; C009281:sodium cyanate