not known. Research indicates that the tachykinin peptide neurokinin B may play a role, as placental expression of the TAC3 gene, which codes for NKB, was found in high levels in women with pre-eclampsia. Usually not located in peripheral tissue, high levels of TAC3 gene were found in both maternal plasma and placental blood, including blood from the umbilical cord. TAC3 in this case was able to secrete NKB in order to affect the circulation of the fetus. Additional studies done on rodents introduced to high levels of NKB indicated the vasoregulatory properties of the peptide, such as the vasoconstriction found in cases of pre-eclampsia. Increased NKB secretions seem to be caused by defective implantation or invasion of the embryo at the trophoblast stage. In most cases of pre-eclampsia, the trophoblast was unable to fully invade into the uterine lining and has been an almost constant feature in documented cases. This leads to increased signaling of NKB factors. In cases of defective implantation, NKB is vital to increase blood flow to the placenta. However, it seems as though depending on which receptor NKB binds, the peptide can cause both constriction and dilation of the blood vessels. The NK1 receptor was studied and found to cause vasodilation while the NK3 receptor was found to cause vasoconstriction. Higher levels of NK3 receptor seem to be found in pregnant woman suffering from pre-eclampsia. NKB usually found in the brain, has been found in the placenta at a concentration of 2.6 times that of the NKB in the brain, possibly leading to the onset of pre-eclampsia in mothers. Studies in non-human animals Much like the human TAC3 gene, Tac2 in rodents facilitates the expression of the neurokinin B peptide. Rodent studies have been done and compared to human studies to elucidate the function of NKB. For cases in which human studies are not possible, rodent studies are substituted due to the conserved similarity between TAC3 and Tac2, and NKB with the TAC3R and Tac2r receptor genes. Studies show that in postmenopausal woman there is an increased expression of tachykinin neurons in the arcuate nucleus. In order to replicate the condition of the post-menopausal woman, an ovariectomized rat is used. The removal of the ovaries simulates the condition of menopause in rats and allows for comparative studies to be done. It was found that in these ovariectomized rats there was a significant increase in the