Acute alcohol consumption causes deficits in motor coordination and gait, suggesting an involvement of cerebellar circuits, which play a role in the fine-adjustment of movements and in motor learning. It has previously been shown that ethanol modulates inhibitory transmission in the cerebellum and affects synaptic transmission and plasticity at excitatory climbing fiber (CF) to Purkinje cell synapses. However, it has not been examined thus far how acute ethanol application affects long-term depression (LTD) and long-term potentiation (LTP) at excitatory parallel fiber (PF) to Purkinje cell synapses, which are assumed to mediate forms of cerebellar motor learning. To examine ethanol effects on PF synaptic transmission and plasticity, we performed whole-cell patch-clamp recordings from Purkinje cells in rat cerebellar slices. We found that ethanol (50mM) selectively blocked PF-LTD induction, while it did not change the amplitude of excitatory postsynaptic currents (EPSCs) at PF synapses. In contrast, ethanol application reduced voltage-gated calcium currents and type-1 metabotropic glutamate receptor (mGluR1)-dependent responses in Purkinje cells, both of which are involved in PF-LTD induction. The selectivity of these effects is emphasized by the observation that ethanol did not impair PF-LTP, and that PF-LTP could readily be induced in the presence of the group I mGluR antagonist (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA), or the mGluR1a antagonist (S)-(+)--amino-4-carboxy-2-methylbenzeneacetic acid (LY367385). Taken together, these findings identify calcium currents and mGluR1-dependent signaling pathways as potential ethanol targets and suggest that an ethanol-induced blockade of PF-LTD could contribute to the motor coordination deficits resulting from alcohol consumption.