Abstract

The object of this study was to compare the effects of short photoperiod (SP) and melatonin (MEL) treatment on the reproductive axis in ovariectomized LSH/SsLak hamsters. Animals acclimatized in long photoperiods (LP) (14L:10D) and showing regular estrous cycles were ovariectomized. Half of the operated hamsters received Silastic capsules containing 17-beta estradiol (E2). On the following day the animals were further subdivided into three groups: the animals in one group received daily afternoon injects of melatonin (MEL), those in a second group were given the vehicle, and animals in the third group were transferred from LP to SP (8L:16D). All animals were killed after 30 days. In hamsters without E2 replacement, MEL or SP exposure significantly suppressed serum and pituitary FSH levels, although MEL was more effective in this regard. On the other hand, SP exposure did not change serum FSH levels in animals with E2 implants, whereas MEL effectively suppressed them. SP or MEL reduced serum LH levels to a similar extent in the absence of E2 replacement, yet in animals with E2 implants only MEL significantly lowered LH levels below LP E2-treated controls. This was in contrast to effects on the pituitary where both treatments were equally effective in the depression of LH content. Serum PRL levels were similarly suppressed by MEL or SP exposure in E2-treated hamsters. On the other hand, pituitary PRL levels were not affected by either treatment in animals with E2-containing capsules, whereas SP or MEL treatment both significantly depressed pituitary PRL contents in hamsters without E2 replacement. SP treatment lowered MBH LHRH contents in animals with E2-containing capsules; no other significant changes in hypothalamic LHRH were noted. The data suggest that daily treatment with 25 micrograms of MEL is generally more effective in the suppression of gonadotropin levels than SP exposure. It is suspected that the mode of administration of MEL, and its quantity, may interact with estrogen differently than SP in the induction of physiological changes and regulation of the LHRH system.

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