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首页> 外文期刊>The European Journal of Neuroscience >Contribution of glial-neuronal interactions to the neuroendocrine control of female puberty.
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Contribution of glial-neuronal interactions to the neuroendocrine control of female puberty.

机译：胶质神经元相互作用对女性青春期神经内分泌控制的贡献。

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摘要

Mammalian puberty is initiated by an increased pulsatile release of the neuropeptide gonadotropin-releasing hormone (GnRH) from hypothalamic neuroendocrine neurons. Although this increase is primarily set in motion by neuronal networks synaptically connected to GnRH neurons, glial cells contribute to the process via at least two mechanisms. One involves production of growth factors acting via receptors endowed with either serine-threonine kinase or tyrosine kinase activity. The other involves plastic rearrangements of glia-GnRH neuron adhesiveness. Growth factors of the epidermal growth factor family acting via erbB receptors play a major role in glia-to-GnRH neuron communication. In turn, neurons facilitate astrocytic erbB signaling via glutamate-dependent cleavage of erbB ligand precursors. The genetic disruption of erbB receptors delays female sexual development due to impaired erbB ligand-induced glial prostaglandin E(2) release. The adhesiveness of glial cells to GnRH neurons involves at least two different cell-cell communication systems endowed with both adhesive and intracellular signaling capabilities. One is provided by synaptic cell adhesion molecule (SynCAM1), which establishes astrocyte-GnRH neuron adhesiveness via homophilic interactions and the other involves the heterophilic interaction of neuronal contactin with glial receptor-like protein tyrosine phosphatase-beta. These findings indicate that the interaction of glial cells with GnRH neurons involves not only secreted bioactive molecules, but also cell-surface adhesive proteins able to set in motion intracellular signaling cascades.
机译：哺乳动物的青春期是由下丘脑神经内分泌神经元的神经肽促性腺激素释放激素（GnRH）的脉冲释放增加引起的。尽管这种增加主要是由与GnRH神经元突触连接的神经元网络推动的，但神经胶质细胞至少通过两种机制参与了这一过程。一种涉及通过赋予丝氨酸-苏氨酸激酶或酪氨酸激酶活性的受体起作用的生长因子的产生。另一个涉及神经胶质-GnRH神经元粘附性的塑性重排。通过erbB受体起作用的表皮生长因子家族的生长因子在神经胶质到GnRH神经元的交流中起主要作用。反过来，神经元通过谷氨酸依赖的erbB配体前体的裂解促进星形细胞erbB信号传导。 erbB受体的基因破坏延迟​​女性性发育，由于受损的erbB配体诱导的神经胶质前列腺素E（2）释放。胶质细胞对GnRH神经元的粘附性涉及至少两个具有粘附和细胞内信号传导能力的不同细胞-细胞通信系统。一种是由突触细胞粘附分子（SynCAM1）提供的，该分子通过同源相互作用建立星形胶质细胞-GnRH神经元的粘附性，另一种涉及神经元接触素与神经胶质受体样蛋白酪氨酸磷酸酶-β的异源相互作用。这些发现表明神经胶质细胞与GnRH神经元的相互作用不仅涉及分泌的生物活性分子，还涉及能够在细胞内信号转导级联反应中起作用的细胞表面粘附蛋白。

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