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 BKCa 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.