The effects of cortisone on acetylcholinesterase (AChE) in the neonatal and aged thymus.

Acetylcholinesterase (AChE) histochemistry and biochemistry was used to characterize the distribution and species of this enzyme within the developing thymus gland of the mouse. The results indicate that AChE-positive nerves and related structures are involved in a steroid-induced mechanism for regulating thymocyte populations. Low doses of cortisone injected into mice produce an activation of quiescent cholinergic nerves and the appearance of several new molecular forms of AChE within areas of the thymus where thymocyte death is prevalent. The action of cortisone on AChE is age dependent. In neonates, AChE activity is extremely high in the cortex of the gland, and cortisone causes little or no increase in AChE activity. In mice three to six weeks old, cortisone exerts its most profound effect on the AChE activity within the thymus. In mice eight months old and older, the AChE activity of the normal thymus is restricted to nerves and nerve-related structures at the cortical-medullary boundaries, with little or no activity observed in the cortex. Injections of cortisone in these mice does not cause an increase in AChE activity in the cortex and only slightly enhances activity within the cortico-medullary boundaries.