Long-term estradiol-17ß administration reduces population of neurons in the sympathetic chain ganglia supplying the ovary in adult gilts.

ABSTRACT

Elevated levels of endogenous estrogens occurring in the course of pathological states of ovaries (follicular cysts, tumors) as well as xenoestrogens may result in hyperestrogenism. In rat, a close relationship between estrogens and sympathetic and sensory neurons supplying the genito-urinary system was reported. Recently, we have shown that long-term estradiol-17ß (E(2)) administration affected morphological and immunochemical organization of the sympathetic ovarian neurons in the caudal mesenteric ganglion of adult gilts. In this study, the influence of E(2) overdose on the number and distribution of neurons in the sympathetic chain ganglia (SChG) projecting to the ovary of adult pigs was investigated. The numbers of ovarian dopamine-ß-hydroxylase (DßH-), neuropeptide Y (NPY-), somatostatin (SOM-), galanin (GAL-) and estrogen receptors (ERs-) immunoreactive perikarya as well as the density of the intraganglionic nerve fibers containing DßH and/or NPY, SOM, GAL were also determined. On day 3 of the estrous cycle the ovaries of both the control and experimental gilts were injected with retrograde neuronal tracer Fast Blue, to identify the neurons innervating gonads. From day 4 of the estrous cycle to the expected day 20 of the second studied cycle, the experimental gilts were injected with E(2), while the control gilts were receiving oil. After the last E(2)/oil injection, the SChG Th16-S2 were collected and processed for double-labeling immunofluorescence. Injections of E(2) (1) increased the E(2) level in the peripheral blood ~4-5 fold, (2) reduced the total number of Fast Blue-positive postganglionic neurons in the ganglia under investigation, (3) decreased the number of perikarya in the L2-L4 ganglia, (4) reduced the number of perikarya in the ventral, dorsal and central regions of the SChG, (5) decreased the numbers of DßH(+)/NPY(+) and DßH(+)/GAL(+) perikarya and the numbers of DßH(+) but NPY(-), SOM(-) and GAL(-) perikarya in the SChG, (6) decreased the number of perikarya expressing ERs subtype α and ß, and (7) decreased the total number of the intraganglionic nerve fibers containing DßH and/or NPY. These results show that long-term E(2) treatment of adult gilts down-regulates the population of both noradrenergic and ERs expressing the SChG ovary supplying neurons. Our findings suggest also that elevated E(2) levels that occur during pathological states may regulate gonadal function(s) by affecting ovary supplying neurons.