Hyperprolactinaemia alleviates behavioral alterations of rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain).

Male rats homozygous for hereditary hypothalamic diabetes insipidus (HO) and their heterozygous (HE) and normal (NO) variants (Brattleboro rats) were made hyperprolactinaemic by homografting two adenopituitaries under the kidney capsule. The high water intake and urine output of homozygous diabetic sham-operated rats (sham-HO) were similar to those of homografted HO animals. Also, hyperprolactinaemia failed to change the water intake and urine output of HE and NO rats, as compared to those of heterozygous (sham-HE) and normal (sham-NO) sham-operated animals. Compared to sham-HE and sham-NO animals, sham-HO rats showed a slow acquisition of active avoidance responses, a facilitated extinction of a pole jumping avoidance behavior and a reduced retention of a passive avoidance response. However, an improved performance of acquisition and retention behaviors up to the level of sham-HEs and sham-NOs was observed in homografted HO rats. Hyperprolactinaemia resulted in a reduced responsiveness to electrical footshock in HO, HE and NO animals, and in facilitated acquisition of active avoidance responses in HE and NO rats, but it failed to affect avoidance extinction and retention in the latter variants. These results suggest that the behavioral alterations shown by homozygous diabetes insipidus rats are alleviated by hyperprolactinaemia although high levels of plasma prolactin do not interfere with the mechanisms regulating water intake and urine output. In addition, hyperprolactinaemia affects the behavior of heterozygous and normal variants of Brattleboro strain but in a selective way.