Baumgartner A, Hiedra L, Pinna G, Eravci M, Prengel H, Meinhold H
Department of Radiological Diagnostic and Nuclear Medicine, Klinikum Benjamin Franklin, Free University of Berlin, Germany.
J Neurochem. 1998 Aug;71(2):817-26. doi: 10.1046/j.1471-4159.1998.71020817.x.
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 (T4) to the active metabolite 3,3',5-triiodo-L-thyronine (T3). As a consequence, the tissue concentrations of T4 fell, and those of T3 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 T3, 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 T3 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.
研究了不同类型的急性应激源对成年雄性大鼠四个脑区（额叶皮质、杏仁核、下丘脑和小脑）以及垂体和肝脏中甲状腺激素浓度和脱碘酶活性的影响。在施加以下每种应激源后处死五组大鼠：(a) 腹腔注射生理盐水，(b) 灌胃，(c) 和 (d) 两种不同形式的处理，即像腹腔注射那样抓握以及从一个笼子转移到另一个笼子，(e) 在缓慢旋转的鼓中放置2小时。另外两组分别在旋转鼓中放置10小时和19小时（睡眠剥夺实验）。所有应激源均导致II型5'-碘甲状腺原氨酸脱碘酶活性显著增加（在某些情况下高达200%），该酶催化前体激素L-甲状腺素（T4）脱碘生成活性代谢物3,3',5-三碘-L-甲状腺原氨酸（T3）。结果，T4的组织浓度下降，T3的浓度上升（有时高达300%）。然而，这些变化仅限于每个应激源所特有的特定脑区，并非在任何组所研究的所有脑区中都能看到。应激对催化T3失活的III型5-碘甲状腺原氨酸脱碘酶同工酶活性、肝脏或血清甲状腺激素浓度或脑I型5'-碘甲状腺原氨酸脱碘酶活性均无明显影响。总之，我们的结果表明，即使是轻微且非常短暂的应激也能特别在脑中而非肝脏或血液中诱导T3浓度显著升高。因此，与普遍观点相反，甲状腺激素可能在应激反应中发挥重要的生理作用，至少在含有II型�'-碘甲状腺原氨酸脱碘酶的组织如脑和垂体中如此。
