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应激对大鼠脑离散结构中N-甲基-D-天冬氨酸识别域的优先诱导作用。

Preferential induction by stress of the N-methyl-D-aspartate recognition domain in discrete structures of rat brain.

作者信息

Yoneda Y, Han D, Ogita K

机构信息

Department of Pharmacology, Setsunan University, Osaka, Japan.

出版信息

J Neurochem. 1994 Nov;63(5):1863-71. doi: 10.1046/j.1471-4159.1994.63051863.x.

Abstract

Immobilization stress in water for 3 h was effective in inducing significant potentiation of 3H-5-methyl-10,11-dihydro-5H- dibenzo [a,d] cyclohepten-5,10-imine ([3H]MK-801) binding 5 days after the stressful manipulation in rat hypothalamus and cerebellum when determined before equilibrium in the absence of any added agonists, in addition to resulting in marked reduction of rearing behaviors of animals. However, the stressful manipulation failed to modulate the [3H]MK-801 binding in other central regions examined, and binding of either [3H]DL-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid or [3H]kainic acid was not significantly affected in all brain structures studied 5 days after the stress application. In contrast, the stressful procedures potentiated binding of both L-[3H]glutamic ([3H]Glu) and [3H]DL-(E)-2-amino-4-propyl-5-phosphono-3-pentenoic ([3H]CGP-39653) acids in the hypothalamus and cerebellum 5 days later, without affecting binding of [3H]-glycine and 5,7-dichloro[3H]kynurenic acid. The systemic administration of corticosterone mimicked the stress manipulation at doses of 5-50 mg/kg in terms of inducing significant enhancement of binding of both [3H]Glu and [3H]CGP-39653 in the hypothalamus and cerebellum when determined 5 days after the single administration. The translation inhibitor cycloheximide was effective in preventing the stress-induced potentiation of [3H]Glu binding in the cerebellum, without altering that in the hypothalamus. Furthermore, the stressful handling significantly increased the densities of [3H]Glu binding sites in the hypothalamus and cerebellum, with the affinities being unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在水中固定应激3小时可有效诱导大鼠下丘脑和小脑中3H-5-甲基-10,11-二氢-5H-二苯并[a,d]环庚烯-5,10-亚胺([3H]MK-801)结合在应激处理5天后显著增强,在无任何添加激动剂的情况下于平衡前测定时,此外还导致动物竖毛行为明显减少。然而,应激处理未能调节所检查的其他中枢区域的[3H]MK-801结合,并且在应激施加5天后,在所研究的所有脑结构中,[3H]DL-α-氨基-3-羟基-5-甲基异恶唑-4-丙酸或[3H] kainic酸的结合均未受到显著影响。相反,应激处理在5天后增强了下丘脑和小脑中L-[3H]谷氨酸([3H]Glu)和[3H]DL-(E)-2-氨基-4-丙基-5-膦酰基-3-戊烯酸([3H]CGP-39653)的结合,而不影响[3H]-甘氨酸和5,7-二氯[3H]犬尿氨酸的结合。皮质酮全身给药在5 - 50mg/kg剂量下模拟了应激处理,在单次给药5天后测定时,诱导下丘脑和小脑中[3H]Glu和[3H]CGP-39653结合显著增强。翻译抑制剂环己酰亚胺可有效阻止应激诱导的小脑中[3H]Glu结合增强,而不改变下丘脑中的情况。此外,应激处理显著增加了下丘脑和小脑中[3H]Glu结合位点的密度,亲和力未变。(摘要截断于250字)

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