Molecular targets for the actions of behaviourally relevant concentrations of alcohol remain elusive. We have identified a class of GABA_A receptors, found in extrasynaptic membranes, which are sensitive to alcohol concentrations achieved after consumption of one drink. One type of these receptors (α6β3δ) is only expressed in cerebellar granule cells where it generates a form of tonic inhibition. We report that low concentrations of alcohol act at these receptors, causing motor impairment. We examined the effects of ethanol on Sprague-Dawley rats bred to be homozygous either for the wild type (α6 ^100R) or for mutant (α6 ^100Q) alleles of a point mutation thought to enhance the alcohol sensitivity of α6 containing GABA receptors; we then used the mutant animals as a tool to investigate the behavioural actions of alcohol at these receptors. We made whole-cell recordings from granule cells in 300μm parasagittal cerebellar slices from humanely killed P24-42 Sprague-Dawley rats. Cells were clamped at -70 mV using CsCl containing pipettes. Homozygous rats (>P55) were tested on an accelerating rotarod test in which the speed of rotation was increased at a constant rate from 4 to 40 rpm over 5 minutes. Data are presented as mean ± S.E.M. Statistical significance was assessed with Student’s t tests or a Wilk’s lambda multivariate test. Tonic GABA conductance in granule cells from both genotypes was sensitive to concentrations of ethanol as low as 10 mM. 30 mM ethanol increased the tonic conductance by 15.7 ± 2.5% (n=5) in wild type granule cells and caused a significantly larger increase (68 ± 11.1%, n=7, P<0.01) in those from α6 ^100Q/Q rats. Moreover mutant animals showed greater motor impairment in response to low doses of ethanol than wild types (P<0.01) n=6 and 7 respectively). 20 minutes after intraperitoneal injection of low doses of ethanol (1g/kg) wild type rats showed only mild motor impairment (the average time that they were able to stay on the rotarod was reduced by 13.1 ± 5.2%, n=6) whereas mutant α6 ^100Q/Q rats were significantly more impaired (27.9 ± 3.6% n=6, P<0.03), suggesting that ethanol enhancement of granule cell tonic inhibition is responsible for alcohol-induced motor impairment. These findings not only identify extrasynaptic GABA_A receptors as a primary alcohol target but also that action at these receptors can account for the effects of alcohol on motor function.