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雄性Fischer 344大鼠大脑皮层和中脑色氨酸羟化酶活性因急性或反复声音应激而增加。

Increase in the activity of tryptophan hydroxylase from cortex and midbrain of male Fischer 344 rats in response to acute or repeated sound stress.

作者信息

Boadle-Biber M C, Corley K C, Graves L, Phan T H, Rosecrans J

机构信息

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

出版信息

Brain Res. 1989 Mar 20;482(2):306-16. doi: 10.1016/0006-8993(89)91193-1.

DOI:10.1016/0006-8993(89)91193-1
PMID:2706489
Abstract

Exposure of male Fischer 344 rats to an acute sound stress consisting of 100 dB tones of 2-s duration presented at random 60-s intervals for 2 h, increased cortical and midbrain tryptophan hydroxylase activity, measured in vitro, 50% over that from sham-stressed animals. This increase in enzyme activity was observed when animals were killed immediately, but not 1 h, after termination of the sound stress. It was non-additive with the increase in activity induced by incubation of enzyme under phosphorylating conditions and could be reversed in vitro with alkaline phosphatase. Graded increases in enzyme activity were obtained with increments of sound intensity (90-120 dB). In contrast to acute stress, chronic sound stress (110 dB) repeated over a period of 1, 2 or 6 weeks (3 sessions per week each of 2-h duration) produced a 50% increase in cortical enzyme activity that persisted 24 h after the termination of the stress and was not reversed by alkaline phosphatase. However, a further increase in enzyme activity could be produced if the chronically stressed animals were exposed to an acute 2-h stress (110 dB) immediately before being killed. This additional increase in activity was reversible in vitro by alkaline phosphatase and non-additive with that produced by incubation under phosphorylating conditions. In summary, acute sound stress produced a prompt, reversible activation of tryptophan hydroxylase. Repeated exposure to sound stress induced a persistent increase in enzyme activity that was detected 24 h after the last stress.

摘要

将雄性Fischer 344大鼠暴露于一种急性声音应激中,该应激由持续2秒、强度为100分贝的音调组成,以随机的60秒间隔呈现2小时,结果显示,体外测量时,其皮质和中脑色氨酸羟化酶活性比假应激动物高出50%。当动物在声音应激结束后立即处死时可观察到这种酶活性的增加,但在应激结束1小时后处死则未观察到。这种增加与在磷酸化条件下孵育酶所诱导的活性增加不具有叠加性,并且在体外可以被碱性磷酸酶逆转。随着声音强度(90 - 120分贝)的增加,酶活性呈梯度增加。与急性应激不同,慢性声音应激(110分贝)在1、2或6周的时间内重复进行(每周3次,每次持续2小时),导致皮质酶活性增加50%,该增加在应激结束后持续24小时,并且不能被碱性磷酸酶逆转。然而,如果在处死前将长期应激的动物立即暴露于急性2小时应激(110分贝)中,则酶活性会进一步增加。这种额外的活性增加在体外可被碱性磷酸酶逆转,并且与在磷酸化条件下孵育所产生的增加不具有叠加性。总之,急性声音应激可迅速、可逆地激活色氨酸羟化酶。反复暴露于声音应激会导致酶活性持续增加,这种增加在最后一次应激后24小时仍可检测到。

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