Influence of Continuous Illumination on Estrous Cycle of Rats: Time Course of Changes in Levels of Gonadotropins and Ovarian Steroids until Occurrence of Persistent Estrus

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Abstract
Plasma concentrations of LH, FSH, 17β-estradiol, estrone and progesterone were determined chronologically by radioimmunoassays in two groups of adult female rats exposed to continuous illumination (LL). Group 1 rats showing vaginal estrous cycles were sacrificed at 3- to 6-hour intervals during late proestrus through early estrus of the first 5 cycles after exposure to LL. Group 2 animals which displayed persistent vaginal estrus in an early period of exposure to LL were killed on the 2nd, 3rd, 4th, 5th and 7th days of vaginal estrus. In Group 1 rats, surges of the hormones, except estrone, took place in all the 5 cycles. The occurrence of peak hormone levels in each cycle was invariably delayed after transfer of animals to LL. According to regression analyses, the lengths of secretion cycles of LH, FSH, 17β-estradiol and progesterone in rats under LL were 100.89, 100.46, 101.14 and 101.06 h, respectively. Elevation of 17β-estradiol levels was observed prior to the LH surge, and peaks of progesterone and FSH occurred following it. However, the secretion patterns of these hormones appear to be disrupted with length of exposure to LL. In group 2 rats, the mean concentration of LH during persistent estrus was approximately similar to that on the morning of the days of proestrus of the 4-day cycles of rats placed under an alternating 12-hour light-dark regimen (LD), whereas the mean FSH concentration was continuously low. While the concentrations of 17β-estradiol and estrone in persistent-estrous rats were elevated, progesterone levels remained low. These findings appear to show that the estrous cycles in LL rats are composed of circaquadridian secretion rhythms, longer than 96 h, of gonadotropins and sex steroids so that the estrous cycles are lengthened and the ovulation is delayed. Prolongation of estrus in LL rats may be accounted for by suppression of the ovulatory surge of LH and consequent decrease in secretion of progesterone caused by continued elevation of blood concentrations of 17β-estradiol.