[Effect of the Ca2+ -activated K+ channel in veratridine-induced cortex neurons damage]

To observe the effects of Ca2+ -activated K+ channel of primary cultured fetal SD rat cortex neurons in the veratridine triggered neuronal damage.

The patch clamp technique of cell-attach and inside-out mode for these two kinds of single channel recordings were used.

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.

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.