Singh V B, Corley K C, Krieg R J, Phan T H, Boadle-Biber M C
Department of Physiology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond 23298.
Eur J Pharmacol. 1994 Apr 21;256(2):177-84. doi: 10.1016/0014-2999(94)90243-7.
The rapidly reversible increase in cortical or midbrain tryptophan hydroxylase activity observed ex vivo after exposure of rats to 1-h sound stress was blocked by hypophysectomy, but not sham hypophysectomy, and restored by dexamethasone administration to the hypophysectomized animals (500 micrograms/day i.p. for 3 days). The response to sound stress was also lost with deafferentation of the hypothalamus. These results indicate that hypothalamic control of adrenal glucocorticoids is required for the serotonergic response to sound stress. The glucocorticoid antagonist, RU 38486, given intracerebroventricularly (200 micrograms/day for 4-5 days) or bilaterally, into the region of the central nucleus of the amygdala (100 micrograms 15 min before stress), blocked the sound stress-induced increase in tryptophan hydroxylase activity. In contrast, the antimineralocorticoid, RU 26752, was without effect. The block obtained with RU 38486 suggests that glucocorticoid is required by the neurons that relay the effects of sound stress to the rostrally projecting serotonergic neurons.
将大鼠暴露于1小时声音应激后，在体外观察到的皮质或中脑色氨酸羟化酶活性迅速可逆性增加，被垂体切除术阻断，但假垂体切除术未阻断，并且通过给垂体切除的动物腹腔注射地塞米松（500微克/天，共3天）得以恢复。下丘脑传入神经切断后，对声音应激的反应也消失了。这些结果表明，血清素能对声音应激的反应需要下丘脑对肾上腺糖皮质激素的控制。糖皮质激素拮抗剂RU 38486，经脑室内给药（200微克/天，共4 - 5天）或双侧给药至杏仁核中央核区域（应激前15分钟给药100微克），可阻断声音应激诱导的色氨酸羟化酶活性增加。相比之下，抗盐皮质激素RU 26752则没有效果。用RU 38486获得的阻断作用表明，将声音应激的影响传递给向前投射的血清素能神经元的神经元需要糖皮质激素。
