GABAA receptors are expressed throughout the CNS, with different receptor subtypes providing heterogeneous expression throughout distinct brain regions. Whilst the exact neural basis for the sedative and ataxic affects of ethanol is currently unknown, the α2-subunit is expressed within brain areas involved in motor output, namely the striatum, cerebellum [29], [30] and within the dorsal and ventral horns of the spinal cord [31], [32], making these the most likely loci to mediate acute sedative/ataxic effects.
