A moderately high concentration of ethanol (50mM) has also been shown to increase the frequency of sIPSCs and to enhance paired-pulse facilitation of evoked IPSCs in dissociated rat cerebellar Purkinje neurons [14]. Medium ethanol concentrations (40mM) also increase the frequency and regularity of spontaneous Golgi cell (interneuron) firing and depolarize the membrane potential of these cells [15]. These effects appear to be the result of an ethanol-induced inhibition of the Na+/K+ ATPase, which controls Golgi cell firing. [12]. This group also demonstrated that moderately high concentrations of ethanol (25 and 50mM) significantly decrease complex spike area in Purkinje cells. At 50mM, ethanol also modulates the late phase of the complex spike, decreasing the amplitude of the after-hyperpolarization, with no effect on calcium transients elicited by climbing fiber stimulation. Application of an mGluR1 receptor antagonist mimicked and occluded the effect on 50mM ethanol on complex spike area, suggesting that interaction with mGluR1 receptors may mediate the effect of ethanol observed in these cells. In support of this, 50mM ethanol inhibited mGluR1-dependent EPSCs recorded from Purkinje neurons in response to climbing fiber
