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胶质细胞向神经元的信号传递与女性青春期的神经内分泌控制。

Glia-to-neuron signaling and the neuroendocrine control of female puberty.

作者信息

Ojeda Sergio R, Prevot Vincent, Heger Sabine, Lomniczi Alejandro, Dziedzic Barbara, Mungenast Alison

机构信息

Division of Neuroscience, Oregon National Primate Research Center/Oregon Health & Science University, Beaverton, Oregon 97006, USA.

出版信息

Ann Med. 2003;35(4):244-55. doi: 10.1080/07853890310005164.

DOI:10.1080/07853890310005164
PMID:12846266
Abstract

The sine qua non event of puberty is an increase in pulsatile release of gonadotrophin hormone releasing hormone (GnRH). It is now clear that this increase and, therefore, the initiation of the pubertal process itself, require both changes in transsynaptic communication and the activation of glia-to-neuron signaling pathways. While neurons that utilize excitatory and inhibitory amino acids as transmitters represent major players in the transsynaptic control of puberty, glial cells utilize a combination of trophic factors and small cell-cell signaling molecules to regulate neuronal function and, thus, promote sexual development. A coordinated increase in glutamatergic transmission accompanied by a decrease in inhibitory GABAergic tone appears to initiate the transsynaptic cascade of events leading to the pubertal increase in GnRH release. Glial cells facilitate GnRH secretion via cell-cell signaling loops mainly initiated by members of the EGF and TGF- families of trophic factors, and brought about by either these factors themselves or by chemical messengers released in response to growth factor stimulation. In turn, a neuron-to-glia communication pathway mediated by excitatory amino acids serves to coordinate the simultaneous activation of transsynaptic and glia-to-neuron communication required for the advent of sexual maturity. A different--and perhaps higher--level of control may involve the transcriptional regulation of subordinate genes that, by contributing to neuroendocrine maturation, are required for the initiation of the pubertal process.

摘要

青春期的必要条件是促性腺激素释放激素(GnRH)脉冲式释放增加。现在已经明确,这种增加以及青春期过程本身的启动,既需要跨突触通讯的变化,也需要胶质细胞到神经元信号通路的激活。虽然利用兴奋性和抑制性氨基酸作为递质的神经元是青春期跨突触控制的主要参与者,但胶质细胞利用营养因子和小细胞间信号分子的组合来调节神经元功能,从而促进性发育。谷氨酸能传递的协同增加伴随着抑制性γ-氨基丁酸能张力的降低,似乎启动了导致GnRH释放青春期增加的跨突触事件级联反应。胶质细胞通过主要由表皮生长因子(EGF)和转化生长因子(TGF)家族的营养因子成员启动的细胞间信号环来促进GnRH分泌,这些信号环由这些因子本身或对生长因子刺激作出反应而释放化学信使所引起。反过来,由兴奋性氨基酸介导的神经元到胶质细胞的通讯通路有助于协调性成熟到来所需的跨突触和胶质细胞到神经元通讯的同时激活。一个不同的——也许是更高层次的——控制水平可能涉及到从属基因的转录调控,这些基因通过促进神经内分泌成熟,是青春期过程启动所必需的。

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