Schwartz M H
Brain Res. 1985 Apr 22;332(2):337-53. doi: 10.1016/0006-8993(85)90602-x.
The subthreshold currents in bursting pacemaker neurons of the Aplysia abdominal ganglion were individually studied with the voltage clamp technique for sensitivity to 4% ethanol. The most prevalent effect of ethanol on unclamped bursting neurons was a hyperpolarization. This was shown to be due to a decrease of a voltage independent inward leakage current. Direct measurement of the Na-dependent slow inward current showed that this current was eliminated by 4% ethanol. Direct measurement of the Ca-dependent slow inward current showed that this current was substantially reduced by 4% ethanol. Injection of EGTA into cell bodies did not eliminate the ethanol-induced block of the slow inward calcium current. Thus, ethanol cannot be reducing the Ca-dependent slow inward current solely by an increase of internal calcium concentration. The effect of ethanol on voltage dependent outward current was measured by blockage of all inward current. The peak outward current was increased by ethanol. The rate of inactivation of this outward current was also increased. Calcium activated potassium current (IK(Ca)) is particularly complicated in its response to ethanol because it is dependent on both Ca and voltage for its activation. The level of IK(Ca) elicited in response to constant Ca injection was increased by ethanol treatment. The level of this current as activated by voltage clamp pulses was either increased or decreased depending on the neuron type. Ca2+ activated potassium conductance increased e-fold for a 26 mV depolarization in membrane holding potential. Ethanol decreased this voltage dependence to e-fold for a 55 mV change in potential. This result was interpreted to mean that ethanol shifted an effective Ca2+ binding site of these channels from about halfway through the membrane field to one quarter of the way across. The same theoretical approach allowed the further conclusion that ethanol caused an increased internal free calcium concentration probably by decreasing calcium binding by intracellular buffers.
运用电压钳技术，对海兔腹神经节爆发性起搏神经元中的阈下电流进行了单独研究，以考察其对4%乙醇的敏感性。乙醇对未钳制的爆发性神经元最普遍的作用是超极化。结果表明，这是由于电压非依赖性内向漏电流的减少所致。对钠依赖性慢内向电流的直接测量表明，该电流被4%乙醇消除。对钙依赖性慢内向电流的直接测量表明，该电流被4%乙醇大幅降低。向细胞体中注入乙二醇双乙醚四乙酸（EGTA）并不能消除乙醇诱导的慢内向钙电流阻断。因此，乙醇不可能仅通过增加细胞内钙浓度来降低钙依赖性慢内向电流。通过阻断所有内向电流来测量乙醇对电压依赖性外向电流的影响。乙醇使外向电流峰值增加。该外向电流的失活速率也增加。钙激活钾电流（IK(Ca)）对乙醇的反应特别复杂，因为其激活既依赖于钙又依赖于电压。乙醇处理使响应恒定钙注入而引发的IK(Ca)水平增加。该电流由电压钳脉冲激活后的水平根据神经元类型而增加或降低。在膜钳制电位去极化26 mV时，Ca2+激活的钾电导增加e倍。乙醇使这种电压依赖性降低，在电位变化55 mV时增加e倍。该结果被解释为意味着乙醇将这些通道的有效Ca2+结合位点从膜电场的大约一半位置转移到了跨膜四分之一的位置。同样的理论方法还得出了进一步的结论，即乙醇可能通过减少细胞内缓冲剂对钙的结合而导致细胞内游离钙浓度增加。
