**4. Discussion**

In the present study we showed that in adult female rats, the effects of E2 on SOM-ir cell distribution and SOM-ir numbers in the PeVN were age dependent. Estrogen did not affect total numbers of SOM-ir cells in the PeVN of young female rats in line with our previous studies (Van Vugt et al, 2008) and those of others (Estupina et al, 1996). Other studies reported a decrease in SOM mRNA content in the PeVN following OVX which was reversed by E2 treatment (Baldino et al, 1988; Zorilla et al, 1991). In these studies, however, animals were treated with E2 for a prolonged period of time, whereas we studied the effect of a single physiological dose of E2 on SOM peptide-containing cells on multiple time points following the estrogen exposure. Interestingly, the amount of SOM-ir fibers within the PeVN region of young females was decreased at 32 h compared to 2 h after E2, which may suggest increased release of SOM peptide from the PeVN or decreased transport from cells to the fibers, apparently without affecting the amount of SOM peptide synthesized and/or stored in the PeVN cells. Prior to measuring SOM peptide responsiveness to an estrogen stimulus we showed that the attenuation of the LH surge at middle-age was not accompanied by a decrease in proestrus P levels or a decrease in pituitary LH responsiveness to a GnRH analog. These results clearly suggest that the attenuation of the LH surge is not initiated by alterations at the level of the ovary or pituitary gland, but rather the result of changes in response to ovarian feedback at the hypothalamic level as found for SOM peptide in this study. Subsequent experiments in the brain material obtained from these animals are now focusing on studying potential changes in hypothalamic estrogen and progesterone receptor immunoreactivity.
