Abstract:
Central administration of neurokinin B (NKB) agonists stimulates immediate early gene
expression in the hypothalamus and increases secretion of vasopressin from the posterior
pituitary through a mechanism that depends on the activation of neurokinin receptor 3
receptors (NK3R). Here we report that, in the rat, immunoreactivity for NK3R is expressed in
magnocellular vasopressin and oxytocin neurones in the supraoptic nucleus (SON) and
paraventricular nucleus (PVN) of the hypothalamus, and that NKB immunoreactivity is
expressed in fibres in close juxtaposition with vasopressin neurones at both of these sites.
Retrograde tracing in the rat showed that some NKB-expressing neurones in the arcuate
nucleus project to the SON, and in mice, using an anterograde tracing approach, we found
that kisspeptin-expressing neurones of the arcuate nucleus, which are known to co-express
NKB, project to the SON and PVN. Finally, we show that i.c.v. injection of the NK3R agonist senktide potently increases the electrical activity of vasopressin neurones in the SON
in vivo with no significant effect detected on oxytocin neurons. The results suggest that NKBcontaining
neurones in the arcuate nucleus regulate the secretion of vasopressin from
magnocellular neurones in rodents, and we discuss the possible significance of this.
