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大鼠皮质和中脑中色氨酸羟化酶活性因急性或反复的声音应激而增加,这种增加可被肾上腺切除术阻断,并可通过地塞米松治疗恢复。

Increases in the activity of tryptophan hydroxylase from rat cortex and midbrain in response to acute or repeated sound stress are blocked by adrenalectomy and restored by dexamethasone treatment.

作者信息

Singh V B, Corley K C, Phan T H, Boadle-Biber M C

机构信息

Department of Physiology, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.

出版信息

Brain Res. 1990 May 14;516(1):66-76. doi: 10.1016/0006-8993(90)90898-l.

DOI:10.1016/0006-8993(90)90898-l
PMID:2364282
Abstract

Exposure of male Sprague-Dawley rats to acute sound stress (2 s, 110 dB sound pulses presented randomly every minute for 1 h) increases the in vitro activity of cortical and midbrain tryptophan hydroxylase by an alkaline phosphatase-reversible mechanism. Repeated exposure to sound stress on three separate days produces a stable increase in enzyme activity that persists 24 h after the termination of the stress and is insensitive to alkaline phosphatase. Adrenalectomy abolishes both increases in enzyme activity to acute or repeated sound stress but does not change baseline levels of enzyme activity. The synthetic glucocorticoid, dexamethasone, (500 micrograms/day i.p.) given for 3 days or 5 out of 6 days, starting day 3 after adrenalectomy, restores the increases in enzyme activity in adrenalectomized rats exposed, respectively, to acute or repeated sound stress. The mineralocorticoid, aldosterone (5 micrograms/day s.c.), does not substitute for dexamethasone in acutely sound-stressed, adrenalectomized rats. Dexamethasone does not alter control levels of enzyme activity in either adrenalectomized rats or rats with intact adrenals (sham-adrenalectomized), but is required to allow the increase in enzyme activity in response to acute or repeated sound stress to be expressed. The effect of the glucocorticoid, thus, appears to be a permissive one.

摘要

将雄性斯普拉格-道利大鼠暴露于急性声音应激(2秒,每分钟随机呈现110分贝的声音脉冲,持续1小时),可通过一种碱性磷酸酶可逆机制提高皮质和中脑色氨酸羟化酶的体外活性。在三个不同的日子里反复暴露于声音应激会使酶活性稳定增加,这种增加在应激终止后24小时仍然存在,并且对碱性磷酸酶不敏感。肾上腺切除术可消除急性或反复声音应激引起的酶活性增加,但不会改变酶活性的基线水平。从肾上腺切除术后第3天开始,给予合成糖皮质激素地塞米松(500微克/天,腹腔注射)3天或6天中的5天,可恢复分别暴露于急性或反复声音应激的肾上腺切除大鼠的酶活性增加。盐皮质激素醛固酮(5微克/天,皮下注射)在急性声音应激的肾上腺切除大鼠中不能替代地塞米松。地塞米松不会改变肾上腺切除大鼠或肾上腺完整(假肾上腺切除)大鼠的酶活性对照水平,但对于响应急性或反复声音应激的酶活性增加的表达是必需的。因此,糖皮质激素的作用似乎是一种允许性作用。

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