Among the three microarray probes, only clone 300899 showed increased expression in alcoholics (5, 6). This suggested a specific GABAB1 splicing change is related with chronic alcohol exposure. Signal intensities of the three probes were different, and the difference was not explicable based on known splicing variants. This suggested that unknown GABAB1 splicing variants are differentially expressed in alcoholic brain. Single nucleotide polymorphisms (SNPs) near splicing sites also alter splicing and may be associated with alcoholism (11-13). Chronic ethanol exposure and withdrawal increased 5’ splice variant expression of the N-Methyl-D-aspartic acid receptor subunit, NR1, without NR1 3’ variant expression changes (14). The L-type voltage-gated Ca2+ channel, α1c, has two splice variants, α1c-1 and α1c-2; chronic ethanol treatment enhanced splicing resulting in a specific increase in the α1c-1 population (15). Other studies have also shown that splicing changes in brain can contribute to a wide range of neuropsychiatric disorders (11).
