Kisspeptin is a potent regulator of the hypothalamo-pituitary-gonadal axis. The 
activation of several vernal and pubertal behaviors involves the action of 
locally synthesized estradiol by hypothalamic aromatase-expressing neurons. 
Little is known about kisspeptin in non-mammalian systems, and its interaction 
with aromatase remains unexamined. The Mallard drake is a seasonal breeder and 
an excellent model for studying the neural mechanisms that regulate the HPG. The 
goals of these studies were to determine (a) if and how kisspeptin regulates the 
drake HPG, (b) if kisspeptin and aromatase are expressed in the Mallard brain, 
and (c) if kisspeptin is co-localized or in apposition with, aromatase- and 
gonadotropin hormone releasing hormone (GnRH) positive neurons. Central 
kisspeptin administration increased plasma luteinizing hormone, an effect 
blocked by pretreatment with the GnRH antagonist, acyline, suggesting a 
conservation of kisspeptin function and mechanism of action in birds and 
mammals. The distribution of kisspeptin in the mallard brain was examined with 
immunocytochemistry (ICC). Neurons that express kisspeptin-like immunoreactive 
(ir) protein were observed in the medial preoptic nucleus (POM) and in ir fibers 
throughout the drake brain. Virtually all POM kisspeptin-ir soma also expressed 
aromatase-ir, suggesting that autocrine mechanisms may predominate in the 
interaction between steroid provision and kisspeptin expression. No 
co-localization was observed between KP-ir and GnRH-ir, although both were 
easily detected in close-proximity in the tuberoinfundibular area. Taken 
together, these data suggest that in the drake, estradiol synthesized by 
aromatase and kisspeptin co-expressing POM neurons may regulate the HPG via an 
effect on GnRH secretion.