In humans and mice, inactivating mutations in fibroblast growth factor receptor 1 () lead to gonadotropin-releasing hormone (GnRH) deficiency and a host of downstream reproductive disorders. It was unclear if Fgfr1 signaling directly upon GnRH neurons critically drove the establishment of a functional GnRH system. To answer this question, we generated a mouse model with a conditional deletion of in GnRH neurons using the Cre/loxP approach.
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