
魚類の生殖過程は、異なるニューロペプチドによって制御されている。濾胞発生はコレシストキニン(CCK)によって、排卵はゴナドトロピン放出ホルモン(GnRH)によって主に調節されている。


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Life histories of oviparous species dictate high metabolic investment in the process of gonadal development leading to ovulation. In vertebrates, these two distinct processes are controlled by the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH), respectively. While it was suggested that a common secretagogue, gonadotropin-releasing hormone (GnRH), oversees both functions, the generation of loss-of-function fish challenged this view. Here we reveal that the satiety hormone cholecystokinin (CCK) is the primary regulator of this axis in zebrafish. We found that FSH cells express a CCK receptor, and our findings demonstrate that mutating this receptor results in a severe hindrance to ovarian development. Additionally, it causes a complete shutdown of both gonadotropins secretion. Using in-vivo and ex-vivo calcium imaging of gonadotrophs, we show that GnRH predominantly activates LH cells, whereas FSH cells respond to CCK stimulation, designating CCK as the bona fide FSH secretagogue. These findings indicate that the control of gametogenesis in fish was placed under different neural circuits, that are gated by CCK.

### Competing Interest Statement

The authors have declared no competing interest.

The satiety hormone cholecystokinin gates reproduction in fish by controlling gonadotropin secretion

魚類の濾胞発生と排卵は異なるニューロペプチドによって制御される