We examined whether a different maternal genotype might differentially affect the brain adrenocorticoid receptor in homozygous diabetes insipidus Brattleboro rats. Two distinct homozygous diabetic offsprings were studied in comparison with Long Evans (LE) rats: one born of a homozygous mother (DI/HOM MOTHER), and the other born of a heterozygous mother (DI/ HET MOTHER). The number of type I adrenocorticoid receptors of DI/HET MOTHER rats was significantly lower than that of LE rats in the hippocampus and hypothalamus, while in the amygdala both type I and type II receptors decreased. Surprisingly, the binding capacity of DI/HOM MOTHER rats, notwithstanding the absence of vasopressin (VP), as in the DI/HET MOTHER, did not differ from that of LE. Superimposable results were obtained in all the brain regions examined. No differences in binding affinity values (K<sub>d</sub>) were detected. It was hypothesized that an ‘unknown factor’ linked to the genotype of the homozygous diabetic mother might counterbalance the receptor deficit otherwise induced by the lack of VP. The existence of two subpopulations of diabetic Brattleboro rats, as used in this study, should prompt to reexamine the origins of some behavioral and endocrine discrepancies appearing in studies on the homozygous diabetes insipidus Brattleboro strain.