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Acute noise stress in rats increases the levels of diazepam binding inhibitor (DBI) in hippocampus and adrenal gland.

作者信息

Ferrarese C, Mennini T, Pecora N, Gobbi M, Appollonio I, Bernasconi P, Frigo M, Regondi C, Pierpaoli C, Frattola L

机构信息

Clinica Neurologica, Universitá di Milano, Monza, Italy.

出版信息

Psychopharmacology (Berl). 1991;103(3):339-42. doi: 10.1007/BF02244287.

DOI:10.1007/BF02244287
PMID:2057538
Abstract

We investigated the effect of acute noise-induced stress on the concentrations of diazepam binding inhibitor (DBI) and its processing products in brain regions and adrenal glands of rats. DBI levels in hippocampus began to increase at 15 and 30 min and became significantly higher (+100%) at 90 and 120 min after stress; they returned to normal values at 360 min. While basal DBI levels were similar in the left and right hippocampus, the stress-induced increase of DBI levels was significantly higher in the left compared to the right side. A significant increase was also detected in the adrenals; here, the time course of DBI increase paralleled that of previously reported plasma corticosterone in stressed rats, being significantly higher 30 min after stress, and recovering to normal values at 60 and 90 min. After acute noise-induced stress, no significant change of DBI levels was detectable in cerebral cortex, striatum, hypothalamus and cerebellum. The present study reports for the first time the occurrence of a modification of DBI and its processing products (ODN-like immunoreactivity) in an experimental model of stress, and suggests a role for these neuropeptides in emotional responses.

摘要

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1
Acute noise stress in rats increases the levels of diazepam binding inhibitor (DBI) in hippocampus and adrenal gland.
Psychopharmacology (Berl). 1991;103(3):339-42. doi: 10.1007/BF02244287.
2
Diazepam binding inhibitor (DBI) increases after acute stress in rat.大鼠急性应激后地西泮结合抑制剂(DBI)增加。
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Benzodiazepine receptors in rat cerebral cortex and hippocampus undergo rapid and reversible changes after acute stress.急性应激后,大鼠大脑皮层和海马体中的苯二氮䓬受体发生快速且可逆的变化。
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Isolation, characterization, and purification to homogeneity of an endogenous polypeptide with agonistic action on benzodiazepine receptors.一种对苯二氮䓬受体具有激动作用的内源性多肽的分离、特性鉴定及纯化至均一性。
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Characterization of peripheral-type benzodiazepine binding sites in brain using [3H]Ro 5-4864.
乙醇戒断所致社交互动减少的应激敏化:促肾上腺皮质激素释放因子-1、苯二氮䓬受体拮抗剂及5-羟色胺1A受体激动剂的抑制作用
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Cerebral lateralization. Biological mechanisms, associations, and pathology: I. A hypothesis and a program for research.大脑半球偏侧化。生物学机制、关联及病理学:I. 一种假说及研究计划。
Arch Neurol. 1985 May;42(5):428-59. doi: 10.1001/archneur.1985.04060050026008.
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Cerebral lateralization. Biological mechanisms, associations, and pathology: II. A hypothesis and a program for research.大脑半球偏侧化。生物学机制、关联及病理学:II. 一项研究假设与研究计划。
Arch Neurol. 1985 Jun;42(6):521-52. doi: 10.1001/archneur.1985.04060060019009.
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Subcellular location and neuronal release of diazepam binding inhibitor.地西泮结合抑制剂的亚细胞定位与神经元释放
J Neurochem. 1987 Apr;48(4):1093-102. doi: 10.1111/j.1471-4159.1987.tb05632.x.
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Increase of peripheral type benzodiazepine binding sites in kidney and olfactory bulb in acutely stressed rats.急性应激大鼠肾脏和嗅球中外周型苯二氮䓬结合位点增加。
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Protracted treatment with diazepam increases the turnover of putative endogenous ligands for the benzodiazepine/beta-carboline recognition site.地西泮的长期治疗会增加苯二氮䓬/β-咔啉识别位点假定内源性配体的更新率。
Proc Natl Acad Sci U S A. 1987 Mar;84(5):1444-8. doi: 10.1073/pnas.84.5.1444.