Abstract: The alcohol‐sensitive (ANT) rat line, developed for high behavioral sensitivity to ethanol, also exhibits enhanced sensitivity to benzodiazepines, such as diazepam. The rat line carries a point mutation in the cerebellum‐specific γ‐aminobutyric acid type A (GABA) receptor subunit α6, making their diazepam‐insensitive (DIS) receptors sensitive to diazepam. We now report that phenotypes of individual ANT and alcohol‐insensitive rats, classified on diazepam sensitivity of cerebellar [H]Ro 15‐4513 binding, correlated well with homozygous wild‐type, homozygous mutant, and heterozygous genotypes, although some heterozygotes were biased toward the parental phenotypes. GABA down‐modulated DIS [H]Ro 15‐4513 binding in mutant homozygotes but tended to up‐modulate it in heterozygotes and wild‐type homozygotes. Slopes for GABA inhibition of cerebellar t‐butylbicyclophosphoro[S]thionate binding were larger in mutant than in wild‐type homozygotes, with heterozygotes being intermediate. Diazepam displacement of [H]Ro 15‐4513 binding in heterozygotes revealed three components, with their affinities indistinguishable from those in combined wild‐type and mutant homozygotes. This lack of interaction in DIS binding between wild‐type and mutant α6 subunits was substantiated by experiments on recombinant receptors. The data suggest that the α6 subunit‐containing GABA receptors in the heterozygotes are formed from individual mutant and wild‐type subunits with their relative expression differing from animal to animal. Copyright © 1995, Wiley Blackwell. All rights reserved