Central action of adrenal steroids during stress and adaptation.

Central action of adrenal steroids during stress and adaptation.
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肾上腺类固醇在应激和适应过程中的中枢作用。

DOI:
--
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发表时间:
1990
影响因子:
--
通讯作者:
E. R. D. Kloet
E. R. D. Kloet
中科院分区:
医学4区
文献类型:
--
作者:
J. M. Reul;W. Sutanto;J. Eekelen;J. Rothuizen;E. R. D. Kloet

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皮质类固醇与中枢神经系统中的受体相互作用。这些受体表现出异质性,可区分为皮质酮和醛固酮结合盐皮质激素受体和地塞米松结合糖皮质激素受体。盐皮质激素受体对皮质酮或醛固酮的配体特异性似乎是由共定位的转皮质素和11 β-羟基类固醇脱氢酶决定的。醛固酮选择性盐皮质激素受体似乎存在于室周器官和下丘脑的AV 3V区域,并介导由盐食欲驱动的行为。在海马的神经元中发现最高浓度的盐皮质激素受体。这些边缘系统盐皮质激素受体部位介导皮质酮对大脑过程的紧张性影响。糖皮质激素受体与皮质酮结合的亲和力比盐皮质激素受体低十倍,广泛分布在大脑的神经元和神经胶质细胞中。糖皮质激素受体参与应激反应的终止(负反馈)。涉及糖皮质激素受体mRNA和结合位点的测量的研究已经揭示糖皮质激素受体受到自动调节。在ADX后,糖皮质激素受体浓度增加,但在慢性应激、长期给予糖皮质激素和衰老后减少。糖皮质激素受体浓度的降低可能会损害应激后糖皮质激素的负反馈作用。ADX后,盐皮质激素受体结合急剧上调,并在ADX后7至24小时达到最大值。盐皮质激素受体mRNA水平在ADX后出现一过性升高。长期ADX对盐皮质激素受体浓度没有影响,但有趣的是,长期地塞米松治疗导致盐皮质激素受体上调。盐皮质激素受体水平在衰老时降低,但这种与年龄相关的减少可以通过用ACTH 4 -9类似物ORG 2766长期治疗来逆转。在功能上,盐皮质激素受体和糖皮质激素受体参与应激反应组织的不同方面,并且它们共同控制动物的应激反应。
Corticosteroids interact with receptors in the central nervous system. These receptors display heterogeneity and can be distinguished as corticosterone- and aldosterone-binding mineralocorticoid receptors and dexamethasone-binding glucocorticoid receptors. Ligand specificity of mineralocorticoid receptors for either corticosterone or aldosterone seems to be determined by co-localized transcortin and the enzyme, 11 beta-hydroxysteroid dehydrogenase. Aldosterone-selective mineralocorticoid receptors appear to be present in the circumventricular organs and the AV3V region of the hypothalamus and mediate behavior that is driven by salt appetite. Highest concentrations of mineralocorticoid receptors are found in neurons of the hippocampus. These limbic mineralocorticoid receptor sites mediate tonic influences of corticosterone on brain processes. Glucocorticoid receptors bind corticosterone with a tenfold lower affinity than do mineralocorticoid receptors, and are widely distributed in neuronal and glial cells of the brain. Glucocorticoid receptors are involved in the termination of the stress response (negative feedback). Studies involving measurement of glucocorticoid receptor mRNA and binding sites have revealed that glucocorticoid receptors are subject to autoregulation. After ADX, glucocorticoid receptor concentration increases, but is reduced after chronic stress, chronic administration of glucocorticoids, and at senescence. A diminished glucocorticoid receptor concentration may compromise the negative feedback action exerted by glucocorticoids after stress. After ADX, mineralocorticoid receptor binding is acutely up-regulated and reaches its maximum between 7 and 24 hours post-ADX. Mineralocorticoid receptor mRNA level shows a transient increase following ADX. Long-term ADX has no effect on the mineralocorticoid receptor concentration, but, interestingly, chronic dexamethasone treatment results in an up-regulation of mineralocorticoid receptors. Mineralocorticoid receptor level is decreased at senescence, but this age-related decrement can be reversed by chronic treatment with the ACTH4-9 analog, ORG 2766. Functionally, mineralocorticoid receptors and glucocorticoid receptors are involved in different aspects of the organization of the stress response, and in conjunction they control the stress responsiveness of the animal.
DOI: 10.1001/archpsyc.1981.01780260017001
发表时间: 1981
影响因子: --
作者:
B. Carroll;M. Feinberg;J. Greden;J. Tarika;A. Albala;R. Haskett;Norman McI. James;Z. Kronfol;N. Lohr;M. Steiner;Jean Paul de Vigne;E. Young
通讯作者: B. Carroll;M. Feinberg;J. Greden;J. Tarika;A. Albala;R. Haskett;Norman McI. James;Z. Kronfol;N. Lohr;M. Steiner;Jean Paul de Vigne;E. Young
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DOI: --
发表时间: 1985
期刊: The Journal of biological chemistry
影响因子: --
作者:
McIntyre,WR;Samuels,HH
通讯作者: Samuels,HH
ACTH 分泌的调节:B 主题的变体。
DOI: 10.1016/b978-0-12-571143-2.50010-1
发表时间: 1987
期刊: Recent progress in hormone research
影响因子: --
作者:
Dallman,MF;Akana,SF;Cascio,CS;Darlington,DN;Jacobson,L;Levin,N
通讯作者: Levin,N
DOI: 10.1007/s11695-008-9616-6
发表时间: 2009-06-01
期刊: OBESITY SURGERY
影响因子: 2.9
作者:
Munoz, Rodrigo;Carvajal, Cristian;Fardella, Carlos
通讯作者: Fardella, Carlos