The absence of a carboxy-terminal tail in the GnRH receptor is not required for the preovulatory luteinizing hormone surge and fertility in mammals.

Genetic loss-of-function approaches and functional calcium imaging reveal cholecystokinin as the primary regulator of follicle-stimulating hormone in zebrafish, redefining our understanding of gonadotropin regulation in vertebrates.

Astrocyte signaling can activate the firing of gonadotropin-releasing hormone neurons and stimulate hormone release.

Neuroanatomical studies reveal presence and cholinergic phenotype of 150,000-200,000 extrahypothalamic gonadotropin-releasing hormone neurons in human basal ganglia and basal forebrain, and RNA-sequencing detects gonadotropin-releasing hormone receptor-1 expression in cholinergic interneurons but not in spiny projection neurons of the human putamen.

The most comprehensive neuroanatomical atlas on the expression of three glycoprotein hormone receptors, namely, TSHRs, LHCGRs, and FSHRs, was mapped using RNAscope, a technology that allows the detection of mRNA at single-transcript level.

Estradiol regulates the pre-ovulatory luteinizing hormone surge through hypothalamic anteroventral periventricular kisspeptin neurons and maintains reproductive cyclicity through arcuate kisspeptin neurons in an activational manner.

Mouse in vivo and in vitro analysis and human genetic screening highlight the role of anti-Müllerian hormone (AMH) signaling in GnRH neuronal development and function, and identify mutations in AMH and AMHR2 in CHH patients.

The arcuate nucleus kisspeptin neurons express multiple transmitters but use only the neuropeptide kisspeptin to drive the episodic secretion of gonadotropin-releasing hormone.

Genetic and pharmacological approaches demonstrate that pituitary adenylate cyclase-activating polypeptide neurons from the ventral premamillary nucleus of the hypothalamus regulate reproductive function by modulating the activity of a subset of Kiss1 neurons in the female mouse.

Many of the synergistic interactions between mutations are modified in the context of unstable proteins in a manner that depends on how the variants promote misfolding in the cell.