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  • Title: Effect of ethanol on subthreshold currents of Aplysia pacemaker neurons.
    Author: Schwartz MH.
    Journal: Brain Res; 1985 Apr 22; 332(2):337-53. PubMed ID: 2581654.
    Abstract:
    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.
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