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新生细胞和皱缩细胞在出生后大鼠齿状回中的肾上腺皮质激素受体表达。

Expression of adrenal steroid receptors by newly born cells and pyknotic cells in the dentate gyrus of the postnatal rat.

机构信息

Laboratory of Neuroendocrinology, Rockefeller University, 1230 York Avenue, New York, New York 10021, USA.

出版信息

Mol Cell Neurosci. 1992 Feb;3(1):44-8. doi: 10.1016/1044-7431(92)90007-o.

DOI:10.1016/1044-7431(92)90007-o
PMID:19912844
Abstract

Neurogenesis and cell survival in the postnatal rat dentate gyrus are regulated by adrenal steroids. Increases in the circulating levels of glucocorticoids and mineralocorticoids result in decreased cell birth and increased cell survival in the dentate gyrus during the first postnatal week. It is presently unknown whether the effects of these hormones on cell birth and survival are direct or indirect. The expression of adrenal steroid receptors by dentate gyrus neuroblasts and pyknotic cells would support the contention that adrenal steroids directly affect neurogenesis and cell death. To determine whether or not this is the case, immunohistochemistry for the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR) was combined with short-survival [(3)H]thymidine autoradiography in rat pups during the first postnatal week. Light microscopic analysis revealed immunoreactivity for both GRs and MRs in the dentate gyrus. Approximately 50% of all pyknotic cells showed GR-like immunoreactivity, whereas no examples of MR-immunoreactive pyknotic cells were detected. In addition, some [(3)H]thymidine-labeled cells were immunoreactive for GRs (approximately 10%) but no [(3)H]thymidine-labeled MR-immunoreactive cells were observed. The relatively high percentage of pyknotic cells that were GR-immunoreactive suggests that adrenal steroids influence cell survival directly through GRs. In contrast, the relatively low percentage of [(3)H]thymidine-labeled cells expressing GRs indicates that adrenal steroids influence cell birth indirectly through an as yet unidentified mechanism.

摘要

神经发生和细胞存活在出生后大鼠齿状回中受肾上腺类固醇调节。循环中糖皮质激素和盐皮质激素水平的增加导致出生后第一周齿状回中细胞生成减少和细胞存活增加。目前尚不清楚这些激素对细胞生成和存活的影响是直接的还是间接的。齿状回神经母细胞和固缩细胞表达肾上腺类固醇受体支持肾上腺类固醇直接影响神经发生和细胞死亡的观点。为了确定是否如此,在出生后第一周的大鼠幼仔中,用糖皮质激素受体 (GR) 和盐皮质激素受体 (MR) 的免疫组织化学方法与短期存活的 [(3)H]胸腺嘧啶放射自显影技术相结合进行了研究。光镜分析显示 GR 和 MR 在齿状回中均有免疫反应性。大约 50%的所有固缩细胞显示出 GR 样免疫反应性,而没有检测到 MR 免疫反应性的固缩细胞。此外,一些 [(3)H]胸腺嘧啶标记的细胞对 GRs 有免疫反应性(约 10%),但没有观察到 [(3)H]胸腺嘧啶标记的 MR 免疫反应性细胞。大量的固缩细胞具有 GR 免疫反应性,这表明肾上腺类固醇通过 GRs 直接影响细胞存活。相比之下,GR 表达的 [(3)H]胸腺嘧啶标记细胞的相对百分比较低表明,肾上腺类固醇通过尚未确定的机制间接影响细胞生成。

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Expression of adrenal steroid receptors by newly born cells and pyknotic cells in the dentate gyrus of the postnatal rat.新生细胞和皱缩细胞在出生后大鼠齿状回中的肾上腺皮质激素受体表达。
Mol Cell Neurosci. 1992 Feb;3(1):44-8. doi: 10.1016/1044-7431(92)90007-o.
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Adrenal steroids regulate postnatal development of the rat dentate gyrus: II. Effects of glucocorticoids and mineralocorticoids on cell birth.肾上腺类固醇调节大鼠齿状回的出生后发育:II. 糖皮质激素和盐皮质激素对细胞生成的影响。
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Adrenal steroid receptor immunoreactivity in cells born in the adult rat dentate gyrus.成年大鼠齿状回中新生细胞的肾上腺类固醇受体免疫反应性
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Blockade of NMDA receptors increases cell death and birth in the developing rat dentate gyrus.阻断NMDA受体可增加发育中大鼠齿状回的细胞死亡和新生。
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Adrenal steroids regulate postnatal development of the rat dentate gyrus: I. Effects of glucocorticoids on cell death.肾上腺类固醇调节大鼠齿状回的出生后发育:I. 糖皮质激素对细胞死亡的影响。
J Comp Neurol. 1991 Nov 15;313(3):479-85. doi: 10.1002/cne.903130308.
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Adult neurogenesis is regulated by adrenal steroids in the dentate gyrus.成年神经发生在齿状回中受肾上腺类固醇调节。
Neuroscience. 1994 Jul;61(2):203-9. doi: 10.1016/0306-4522(94)90224-0.
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Adrenal hormones suppress cell division in the adult rat dentate gyrus.肾上腺激素抑制成年大鼠齿状回中的细胞分裂。
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Differentiation of newly born neurons and glia in the dentate gyrus of the adult rat.成年大鼠齿状回中新生神经元和神经胶质细胞的分化
Neuroscience. 1993 Sep;56(2):337-44. doi: 10.1016/0306-4522(93)90335-d.
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Naturally occurring cell death in the developing dentate gyrus of the rat.大鼠发育中的齿状回中自然发生的细胞死亡。
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The effects of adrenal steroids and excitatory input on neuronal birth and survival.肾上腺类固醇和兴奋性输入对神经元生成与存活的影响。
Ann N Y Acad Sci. 1994 Nov 14;743:73-92; discussion 92-3. doi: 10.1111/j.1749-6632.1994.tb55788.x.

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