Sound stress activation of tryptophan hydroxylase blocked by hypophysectomy and intracranial RU 38486.
Sound stress activation of tryptophan hydroxylase blocked by hypophysectomy and intracranial RU 38486.
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垂体切除术和颅内 RU 38486 可阻断色氨酸羟化酶的声音应激激活。
DOI：
10.1016/0014-2999(94)90243-7
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发表时间：
1994
影响因子：
5
通讯作者：
Boadle-Biber,MC
中科院分区：
文献类型：
--
作者：
Singh,VB;Corley,KC;Krieg,RJ;Phan,TH;Boadle-Biber,MC
大鼠暴露于1小时声音应激后，离体观察到的皮质或中脑色氨酸羟化酶活性的快速可逆增加被垂体切除术阻止，但假垂体切除术却不能阻止，并通过对垂体切除动物给予地塞米松（500 μg/天）恢复。腹腔注射3天）。对声音应激的反应也随着下丘脑的传入神经阻滞而消失。这些结果表明，下丘脑控制肾上腺糖皮质激素是必要的血清能反应声音应激。糖皮质激素拮抗剂RU 38486，脑室注射（200 μg/天，持续4-5天）或双侧杏仁核中央核区注射（应激前15分钟注射100 μg），可阻断声音应激诱导的色氨酸羟化酶活性增加。相反，抗盐皮质激素RU 26752则无作用。用RU 38486获得的阻断表明，糖皮质激素是神经元所必需的，所述神经元将声音应激的作用传递到吻侧投射的肾上腺素能神经元。
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 μg/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 glucocorticoid is required for the serotoenergic response to sound stress. The glucocorticoid antagonist, RU 38486, given intracerebroventricularly (200 μg/day for 4–5 days) or bilaterally, into the region of the central nucleus of the amygdala (100 μg 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.