Reciprocal changes in plasma corticosterone and testosterone in stressed male rats maintained in a visible burrow system: evidence for a mediating role of testicular 11 beta-hydroxysteroid dehydrogenase.

The purpose of these studies was to investigate the possible role of rat Leydig cell 11 beta-hydroxysteroid dehydrogenase (11HSD) in mediating the inhibitory effects of corticosterone on testosterone production. In a unique communal environment, the visible burrow system, male Long-Evans rats spontaneously segregated into unstressed dominant and stressed subordinate social relationships. Subordinate animals had elevated plasma corticosterone and diminished circulating testosterone levels relative to the dominant animals. The categories of animals were distinguished by behavioral criteria: weight change, wounds received, offensive and defensive behavior, and freedom of movement. As a result of their persistently elevated corticosterone levels, subordinate animals had smaller thymi and larger adrenals and spleens than dominants. We have postulated that Leydig cells are protected against the inhibitory effects of glucocorticoids on testosterone secretion by the inactivating effects of 11HSD. High corticosterone and low 11HSD are predicted to suppress testosterone production, and normal or diminished corticosterone levels combined with normal or elevated 11HSD should permit undiminished testosterone production. Consistent with these predictions, the testes of subordinate animals contained significantly lower 11HSD activity than those of dominant animals. The 11HSD of livers of subordinate and dominant animals were statistically indistinguishable. The results of this study support the postulated role of 11HSD as a protector of Leydig cell function.