Rat Brain Type II 5′‐Iodothyronine Deiodinase Activity Is Extremely Sensitive to Stress

The effects of different kinds of acute stressor on thyroid hormone concentrations and deiodinase activities were investigated in four brain regions (frontal cortex, amygdala, hypothalamus, and cerebellum) and in the pituitaries and livers of adult male rats. Five groups of rats were killed after each of the following stressors: (a) an intraperitoneal injection of saline, (b) intragastric intubation, (c) and (d) two different forms of handling, being grasped as for intraperitoneal injection and being moved from one cage to another, and (e) a 2‐h period spent in a slowly rotating drum. Two other groups were placed in the rotating drums for 10 and 19 h (sleep deprivation experiment), respectively. All stressors induced significant (in some cases up to 200%) increases in the activity of type II 5′‐iodothyronine deiodinase, which catalyzes the deiodination of the prohormone l ‐thyroxine (T 4 ) to the active metabolite 3,3′,5‐triiodo‐ l ‐thyronine (T 3 ). As a consequence, the tissue concentrations of T 4 fell, and those of T 3 rose (sometimes by up to 300%). However, these changes were limited to selected areas of the brain that were specific for each stressor and were not seen in all brain regions investigated in any group. No clear‐cut effects of stress were seen on the activities of the type III 5‐iodothyronine deiodinase isoenzyme, which catalyzes the inactivation of T 3 , on liver or serum thyroid hormone concentrations or on liver of brain type I 5′‐iodothyronine deiodinase activities. In summary, our results show that even mild and very brief stress can induce marked increases in T 3 concentrations specifically in brain but not in liver or blood. Thus, contrary to common opinion, thyroid hormones may play an important physiological role in stress reactions, at least in tissues that contain type II 5′‐iodothyronine deiodinase, such as brain and pituitary.