乙醇对颈上神经节神经元钙内流的影响

Effect of Voltage-Dependent Calcium Channels and Ionophore Channels on Cultured Superior Cervical Ganglion by Ethanol

分散、培养新生12 h内大鼠的颈上交感神经节细胞,应用全细胞膜片钳和共聚焦显微技术观察不同浓度乙醇对颈上神经节细胞钙内流的作用.10,30,100,300,600 mmol/L乙醇对钙电流峰值的抑制率依次为0.080±0.031,0.120±0.053,0.277±0.062,0.570±0.082和0.895±0.054.100 mmol/L乙醇可将40 mmol/L KCl诱发的胞浆内钙离子浓度([Ca2+]i)增高从1.725±0.159显著抑制至1.156±0.135,可将1μmol/L钙离子载体A23187诱发的[Ca2+]i增高从2.232±0.015显著抑制至1.263±0.047.故乙醇对交感神经元细胞外钙内流具抑制作用,急性乙醇中毒可能与其抑制钙电流有一定关系.

The effect of ethanol on voltage-dependent calcium channel in the cultured superior cervical ganglion was observed with conventional whole-cell patch clamp technique. Cytoplasmic calcium concentration （[Ca^2±]i） changes caused by ethanol were measured by monitoring the alteration of cell fluorescence. Inhibition rate of calcium current by 10,30,100,300,600 mmol/L ethanol was 0. 080 ± 0. 031,0. 120±0.053,0.277±0.062,0.57±0.082 and 0.895±0.054. But ethanol did not affect the decay of calcium currein, the voltage dependence or the time course of activation. 100 mmol/L ethanol significantly inhibited [Ca^2＋];increments evoked by 40 mmol/I, KC1 from 1.725±0.159 to 1.156±0.135 （F/F0）. Inhibition of 1μmol/L A23187-induced [Ca^2＋]; increment by 100 mmol/L ethanol was significant from 2. 232±0. 015 to 1.263±0.047 （F/F0）. Ethanol inhibits the calcium influx through VDCCs and ionophore channels significantly and dosage dependently.