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Objective: To investigate the effect of batroxobin on K+ channel activated by Ca2+ in primary cultured cortex neurons of fetal SD rat., Methods: The patch clamp technique of single channel recordings including cell-attach and inside-out mode was used., Results: Extracellular batroxobin activated the Kca. In Ca2+ bath solution of cell-attach mode, Vp +30 mV, when the concentrations of batroxobin were 0.15, 0.25, 0.50, 0.75 and 1.0 mmol/L, the open probabilities of the channel were 0.013 +/- 0.002, 0.082 +/- 0.011, 0.131+/- 0.012, 0.211+/- 0.010 and 0.062 +/- 0.009 (P < 0.01), respectively. It appeared concentration-dependent within 0.75 mmol/ L. batroxobin. In Ca2+ free-bath solution of cell-attach mode, Vp+50 mV, when the concentrations of batroxobin were 0.15, 0.40, 0.60 and 1.0 mmol/L, the open probabilities of the channel were 0.013 +/- 0.001, 0.112 +/- 0.007, 0.193 +/- 0.010 and 0.301 +/- 0.009 (P < 0.05), respectively. In the 6 cases of inside-out mode patch clamp, Vp +40 mV, when the concentrations of batroxobin were 0, 0.25 and 0.50 mmol/L, the open probabilities of the channel were 0. 012 +/- 0.007, 0.011 +/- 0.009 and 0.013 +/- 0.008 (P > 0.05), respectively. There was no significant difference in open probabilities, average open/close times and amplitudes at different intracellular batroxobin concentrations., Conclusion: Batroxobin can affect the activation of the Kca channel through regulating the concentration of cytoplasmic free Ca2+. It may have a protective effect on neurons.

Aim: To observe the effects of Ca2+ -activated K+ channel of primary cultured fetal SD rat cortex neurons in the veratridine triggered neuronal damage., Methods: The patch clamp technique of cell-attach and inside-out mode for these two kinds of single channel recordings were used., Results: Extracellular veratridine activated the Kca. In Ca2+ bath solution of cell-attach mode, Vp + 30 mV, when the concentration (micromol/L) of veratridine were 15,25,50 and 75, the open probabilities of the channel were 0.014 +/- 0.003, 0.085 +/- 0.010, 0.132 +/- 0.016 and 0.059 +/- 0.006 (P < 0.01) respectively. It appeared concentration-dependent within 50 micromol/L veratridine. In Ca2+ free bath solution of cell-attach mode, Vp = +50 mV, when the concentration (micromol/L) of veratridine were 15, 40,60 and 100, the open probabilities of the channel were 0.014 +/- 0.010, 0.113 +/- 0.006, 0.141 +/- 0.004 and 0.295 +/- 0.009 (P < 0.05) respectively. In the 6 cases of inside-out mode patch clamp, Vp = +40 mV, when the concentration of veratridine were 0, 25 micromol/L and 50 micromol/L, the open probabilities of the channel were 0.011 +/- 0.008, 0.010 +/- 0.010 and 0.012 +/- 0.007 (P > 0.05) respectively. There were no significant difference on open probabilities, average open/close times and amplitudes at different intracellular veratridine concentration., Conclusion: Veratridine can affect the activation of the Kca channel through regulating the concentration of cytoplasmic free Ca2+. The opening of Kca activated by increase of intracellular Ca2+ during the early stage of anoxia may be a protection reaction of ischemic neurons.