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星形胶质细胞在雌激素对突触可塑性和脑修复的调节中的作用。

Role of astroglia in estrogen regulation of synaptic plasticity and brain repair.

作者信息

Garcia-Segura L M, Naftolin F, Hutchison J B, Azcoitia I, Chowen J A

机构信息

Instituto Cajal, CSIC, Av. Dr. Arce 37, E-28002 Madrid, Spain.

出版信息

J Neurobiol. 1999 Sep 15;40(4):574-84.

PMID:10453057
Abstract

Astroglia are targets for estrogen and testosterone and are apparently involved in the action of sex steroids on the brain. Sex hormones induce changes in the expression of glial fibrillary acidic protein, the growth of astrocytic processes, and the degree of apposition of astroglial processes to neuronal membranes in the rat hypothalamus. These changes are linked to modifications in the number of synaptic inputs to hypothalamic neurons. These findings suggest that astrocytes may participate in the genesis of androgen-induced sex differences in synaptic connectivity and in estrogen-induced synaptic plasticity in the adult brain. Astrocytes and tanycytes may also participate in the cellular effects of sex steroids by releasing neuroactive substances and by regulating the local accumulation of specific growth factors, such as insulin-like growth factor-I, that are involved in estrogen-induced synaptic plasticity and estrogen-mediated neuroendocrine control. Astroglia may also be involved in regenerative and neuroprotective effects of sex steroids, since astroglia formation after brain injury or after peripheral nerve axotomy is regulated by sex hormones. Furthermore, the expression of aromatase, the enzyme that produces estrogen, is induced de novo in astrocytes in lesioned brain areas of adult male and female rodents. Since astroglia do not express aromatase under normal circumstances, the induction of this enzyme may be part of the program of glial activation to cope with the new conditions of the neural tissue after injury. Given the neuroprotective and growth-promoting effects of estrogen after injury, the local production of this steroid may be a relevant component of the reparative process.

摘要

星形胶质细胞是雌激素和睾酮的作用靶点,显然参与了性类固醇对大脑的作用。性激素可诱导大鼠下丘脑胶质纤维酸性蛋白表达、星形胶质细胞突起生长以及星形胶质细胞突起与神经元膜贴附程度的变化。这些变化与下丘脑神经元突触输入数量的改变有关。这些发现表明,星形胶质细胞可能参与成年大脑中雄激素诱导的突触连接性性别差异以及雌激素诱导的突触可塑性的形成。星形胶质细胞和伸长细胞也可能通过释放神经活性物质以及调节特定生长因子(如胰岛素样生长因子-I)的局部积累来参与性类固醇的细胞效应,这些生长因子参与雌激素诱导的突触可塑性和雌激素介导的神经内分泌控制。星形胶质细胞还可能参与性类固醇的再生和神经保护作用,因为脑损伤或周围神经切断术后星形胶质细胞的形成受性激素调节。此外,在成年雄性和雌性啮齿动物受损脑区的星形胶质细胞中,可从头诱导产生雌激素的芳香化酶的表达。由于星形胶质细胞在正常情况下不表达芳香化酶,这种酶的诱导可能是胶质细胞激活程序的一部分,以应对损伤后神经组织的新状况。鉴于损伤后雌激素具有神经保护和促进生长的作用,这种类固醇的局部产生可能是修复过程的一个相关组成部分。

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