Co-localization of estrogen and angiotensin receptors within subfornical organ neurons

A double-staining immunocytochemical study was done in ovariectomized (OVX) female rats that were either treated with 17beta-estradiol (E(2)) (OVX+E(2)) to produce an approximate circulating level of 30 pg/ml plasma, or not-treated with E(2) (OVX), to investigate the distribution of subfornical organ (SFO) neurons that contained estrogen receptors (ER), and to determine whether these neurons also contained the angiotensin II AT(1)-receptor (AT(1)R). Neurons that contained either ER-like immunoreactivity only, AT(1)R-like immunoreactivity only, or both ER and AT(1)R immunoreactivity were found throughout the extent of the SFO in both the OVX+E(2) and OVX rats. However, some regional differences were apparent in both groups of female rats. Neurons containing the ER were predominantly found in the peripheral regions of the SFO, near large blood vessels and the ependymal layer of the third ventricle. A number of lightly stained ER containing neurons was also observed scattered throughout the central core region of the SFO. OVX only animals were found to have a larger number of ER containing neurons in the SFO compared to the E(2) treated animals. Neurons containing AT(1)R were also found throughout the SFO, but without a distinct distribution pattern in either group of rats, although there were more neurons that exhibited AT(1)R immunoreactivity in the OVX animals. Finally, a distinct group of SFO neurons was found that exhibited both ER and AT(1)R immunoreactivity in both groups of animals, although a larger number of these double labelled neurons was found in the OVX animal. Most of these neurons were also found along the peripheral border of the SFO in close proximity to blood vessels and the ventricular lining. These data have demonstrated the co-existence of ER and AT(1)R in SFO neurons of the female rat, and suggest that circulating level of E(2) alter the expression of both the ER and AT(1)R in these neurons. In addition, these data suggest that E(2) may alter the physiological responses of SFO neurons to angiotensin II by down regulating the number of AT(1)R.