Magnocellular vasopressin system in ontogenesis: development and regulation

This review is devoted to the development, functional activity, and regulation of the magnocellular vasopressin (VP) system in ontogenesis. Magnocellular VP neurons originate in embryos from the neuroepithelium of the third ventricle and migrate first to the supraoptic nucleus and then to the paraventricular nucleus and accessory nuclei. The preproVP gene and synthesis are expressed simultaneously in the newly formed neurons either during migration or just after arrival in magnocellular nuclei. Still, a number of VP-immunoreactive neurons increase in immature mammals to prepuberty, which is explained by VP expression in the initially "silent" neurons, or by an increase of VP synthesis that makes a cell distinguishable by immunocytochemistry. An enzymatic processing of preproVP is slightly delayed compared to the onset of preproVP synthesis. Axons of magnocellular neurons reach the pituitary posterior lobe before or just after the neuron arrival in magnocellular nuclei. The mechanisms of VP release from the axon terminals are developed in immature animals over the perinatal period. The VP neurons begin to react to functional (osmotic) stimulation by increased synthesis of VP mRNA and VP in immature animals from the end of fetal life. A functional maturation of the VP system is under control by neural afferents, neuropeptides, and some hormones of endocrine glands. Namely, glucocorticoids, VP, catecholamines, glutamate, and opioids provide short-term or long-lasting effects on differentiating VP neurons. Most of the intercellular signals inhibit the specific phenotype expression of differentiating VP neurons: VP gene and synthesis in normal conditions, as well as TH gene and synthesis under functional stimulation.