Neurons that produce gonadotropin-releasing hormone (GnRH), which control fertility, complete their nose-to-brain migration by birth. However, their function depends on integration within a complex neuroglial network during postnatal development. Here, we show that rodent GnRH neurons use a prostaglandin D₂ receptor DP1 signaling mechanism during infancy to recruit newborn astrocytes that ‘escort’ them into adulthood, and that the impairment of postnatal hypothalamic gliogenesis markedly alters sexual maturation by preventing this recruitment, a process mimicked by the endocrine disruptor bisphenol A. Inhibition of DP1 signaling in the infantile preoptic region, where GnRH cell bodies reside, disrupts the correct wiring and firing of GnRH neurons, alters minipuberty or the first activation of the hypothalamic–pituitary–gonadal axis during infancy, and delays the timely acquisition of reproductive capacity. These findings uncover a previously unknown neuron-to-neural-progenitor communication pathway and demonstrate that postnatal astrogenesis is a basic component of a complex set of mechanisms used by the neuroendocrine brain to control sexual maturation.

产生控制生育能力的促性腺激素释放激素 (GnRH) 的神经元在出生时完成了从鼻到脑的迁移。然而，它们的功能取决于出生后发育过程中复杂神经胶质网络的整合。在这里，我们表明啮齿动物 GnRH 神经元使用前列腺素 D ₂受体 DP1 信号传导机制在婴儿期招募新生星形胶质细胞“护送”他们进入成年期，并且出生后下丘脑胶质生成的损害通过阻止这种招募来显着改变性成熟，内分泌干扰物双酚 A 模拟的过程。 GnRH 细胞体所在的婴儿期视前区破坏了 GnRH 神经元的正确连接和放电，改变了婴儿期的小青春期或下丘脑-垂体-性腺轴的首次激活，并延迟了及时获得生殖能力。这些发现揭示了一种以前未知的神经元到神经祖细胞的通讯途径，并证明出生后的星体发生是神经内分泌大脑用来控制性成熟的一组复杂机制的基本组成部分。