Plasma patterns of LH, FSH and prolactin in rats with a polycystic ovarian condition induced by oestradiol valerate

Abstract

The patterns of plasma LH, FSH and prolactin concentrations were investigated in rats with a polycystic ovary condition (PCO). The condition was induced by treatment with oestradiol valerate 9 weeks before blood sampling. Serial blood samples were taken at 10-min intervals for 4 h from ten rats with PCO. All samples were assayed for LH, those from five animals for FSH and those from the remaining five animals for prolactin. In addition, five control animals with normal oestrous cycles were sampled during oestrus and the samples assayed for LH. Mean concentrations of LH, FSH and prolactin in rats with PCO were 140 ng/l, 76 micrograms/l and 7.6 micrograms/l respectively. All three hormones exhibited an episodic pattern. The mean peak amplitudes of LH, FSH and prolactin were 120 ng/l, 25 micrograms/l and 3.5 micrograms/l respectively. All three hormones exhibited a similar mean frequency of four or five episodes per 4 h. The LH and FSH patterns were closely synchronized; nearly all FSH peaks coincided with LH peaks. The prolactin pattern did not, however, correlate with that of the gonadotrophins. Despite the persistent oestrous condition of the animals with PCO, it was clear that their pattern of LH did not resemble that of cyclic animals in normal oestrus; in the normally cyclic animals in oestrus the pulse period was nearly twice as long and the pulse amplitude was more than sixfold greater than those in animals with PCO. We conclude that the unique episodic patterns of gonadotrophins are more important than mean blood concentrations of these hormones in establishing and maintaining the polycystic ovary syndrome.

Remission of the polycystic ovarian condition (PCO) in the rat following hemiovariectomy

“…To determine how and why this occurs, we have examined the changes in follicle populations at early intervals following hemiovariectomy in animals with PCO. In view of the significance of the plasma LH patterns in PCO (McCarthy et al, 1986Grosser et al, 1987), we would predict that any change in follicular populations should be preceded by a change in the plasma LH pattern. We have, therefore, also examined the plasma LH pattern several hours after hemiovariectomy.…”

“…Clusters of large polygonal secondary interstitial cells are abundant in the stroma (Hemmings et al, 1983;Schulster et al, 1984;Brawer et al, 1986Brawer et al, , 1989). It appears that the expression of this characteristic polycystic morphology does not reflect intrinsic ovarian pathology, but rather is the response of an essentially normal ovary to an abnormal pattern of gonado-0 1990 WILEY-LISS, INC tropin stimulation McCarthy et al, 1986;Grosser et al, 1987;Carriere et al, 1989). Examination of the histological transition from the normal to the polycystic state indicates that the polycystic morphology is really the product of complete or arrested atresia of developing secondary follicles and the absence of ovulation .…”

“…The cysts themselves represent partial or arrested atresia of large secondary follicles or type I11 large follicular structures Desjardins and Brawer, 1989). The processes of follicular recruitment and atresia that produce the polycystic ovary seems to be driven by a specific plasma gonadotropin pattern (McCarthy et al, 1986Grosser et al, 1987).We have shown that cyclicity and normal ovarian morphology can be restored in EV-induced PCO by the removal of one polycystic ovary (i.e., hemiovariectomy) (Farookhi et al, 1985), indicating that the polycystic ovary retains the capacity for normal function. Regular…”

Monosodium Glutamate-lnduced Reductions in Hypothalamic Beta-Endorphin Content Result in Mu-Opioid Receptor Upregulation in the Medial Preoptic Area

“…Evidence from our laboratory indicates that EV treatment produces an in tractable impairment in the hypothalamic pattern of lu teinizing hormone releasing hormone (LH-RH) delivery [3,4] which, in turn, results in selective defects in pituitary LH production, storage, and release [3]. This cascade of hypothalamic and pituitary defects ultimately translates into a unique attenuated plasma pattern of LH, to which the ovaries respond by becoming polycystic [5][6], Our investigation into the nature of the primary hypo thalamic impairment responsible for this cascade of events has revealed significant alterations in opioid func tion. We have shown that 'H-naloxone binding in the anterior hypothalamus is elevated in EV-treated rats [7].…”

Rodent models of polycystic ovary syndrome

“…Young cycling adult rats exposed to E2 for 8 weeks via a subcutaneous continuous release implant [55] or a single injection of estradiol valerate (EV) [56][57][58][59] exhibited acyclicity, anovulation, and polycystic ovaries, which contained an increased number of atretic follicles and cysts with a thin granulosa cell layer and an abnormally thickened theca layer [55,57,60]. However, EV treatment decreased ovary weight and failed to provoke LH hypersecretion [56,61], hyperandrogenism, obesity, and changes in glucose and insulin concentrations, which differs significantly from human PCOS, but rats did exhibit hypertension and an increase in inguinal fat depot weight [60].…”