NK-cell cytotoxic activity and their relative distributions were studied in the spleen of female Lurcher mice with spontaneous olivopontocerebellar degeneration (C3H) and female athymic nu/nu mice (BALB/c) influenced by 3-acetylpyridine (the neurotoxin causing selective degeneration of cerebellar and inferior olive neurons in some rodent species). The congenital olivopontocerebellar degeneration in Lurcher mice is followed by only an insignificant increase of NK-cell cytotoxic activity (1.2 times). On the other hand, the congenital thymic dysgenesis in nu/nu mice is compensated by a substantial increase in cytotoxic activity (19.4-fold). The administration of 3-acetylpyridine (including prevalent neuronal destruction particularly in Lurcher mutants) caused a decrease of NK-cell cytotoxic activities in all groups of mice (in Lurcher and C3H controls to 60 and 50%, respectively, and in nu/nu and BALB/c controls to 25 and 60%). Relative distributions of NK-cells in spleens of non-influenced and influenced animals were not significantly changed. Some fundamental immune mechanisms, such as the NK-cell cytotoxic activity, were demonstrated to be controlled by congenitally determined or artificially induced changes in both the nervous and the immune systems.