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We found a novel sexually dimorphic area (SDA) in the dorsal hypothalamus (DH) of mice. The SDA-DH was sandwiched between 2 known male-biased sexually dimorphic nuclei, the principal nucleus of the bed nucleus of the stria terminalis and the calbindin-sexually dimorphic nucleus, and exhibited a female-biased sex difference in neuronal cell density. The density of neurons in the SDA-DH was increased in male mice by orchidectomy on the day of birth and decreased in female mice by treatment with testosterone, dihydrotestosterone, or estradiol within 5 days after birth. These findings indicate that the SDA-DH is defeminized under the influence of testicular testosterone, which acts via both directly by binding to the androgen receptor, and indirectly by binding to the estrogen receptor after aromatization. We measured the activity of SDA-DH neurons with c-Fos, a neuronal activity marker, in female mice during maternal and sexual behaviors. The number of c-Fos-expressing neurons in the SDA-DH of female mice was negatively correlated with maternal behavior performance. However, the number of c-Fos-expressing neurons did not change during female sexual behavior. These findings suggest that the SDA-DH contains a neuronal cell population, the activity of which decreases in females exhibiting higher performance of maternal behavior, but it may contribute less to female sexual behavior. Additionally, we examined the brain of common marmosets and found an area that appears to be homologous with the mouse SDA-DH. The sexually dimorphic structure identified in this study is not specific to mice and may be found in other species.

ABSTRACT. In the pregnant bitch, the placenta is a major source of circulating relaxin, but its local expression in the reproductive organs is not clear. This study demonstrated expression of relaxin mRNA in the corpus luteum, uterus, uterine cervix as well as placenta in the pregnant and nonpregnant bitch by reverse transcriptase-polymerase chain reaction (RT-PCR).KEY WORDS: canine, corpus luteum, relaxin, uterine cervix, uterus.J. Vet. Med. Sci. 72(10): 1383-1386, 2010 Relaxin is a peptide hormone of about 6 kDa that has been traditionally associated with pregnancy in mammals. The major biological actions of relaxin include inhibition of uterine myometrial contractility [6] and promotion of connective tissue remodeling in the uterine cervix [8]. However, since the physiology of relaxin are richly diverse among species [22], accumulation of knowledge concerning this hormone for a given species is needed. As a fundamental step toward understanding how relaxin initiates its effects, it is important to identify the site of its production.The major source of circulating relaxin is different among species. It is the ovarian corpus luteum in the mouse [2], rat [11,14] [26,31], and mare [28], and the endometrial gland cells of the uterus in the guinea pig [20]. In addition to its hormonal roles during pregnancy, it has been suggested that relaxin has autocrine and paracrine roles in the ovary and uterus. In the ovary, locally produced relaxin may have stimulatory effects on the follicular growth and corpus luteum function [3,19], and it could be possible that relaxin expressed in the uterus acts directly on the inhibition of uterine contractility and the control of collagen remodeling in fetal membranes [5].In the dog, both the placenta and ovary are reported to secrete relaxin, with the placenta being the major contributor to the serum relaxin levels during pregnancy [26,31]. Klonisch et al. [16] showed the nucleic acid sequence of canine preprorelaxin cDNA and the localization of the mRNA and its protein in the syncytiotrophoblasts of the placenta. However, local expression of relaxin in the reproductive organs of the bitch remains to be elucidated. This study examined expression of relaxin mRNA in the corpus luteum, uterus and uterine cervix in the bitch.Ovaries, uteri, uterine cervices or placentae were taken from 12 bitches. There were 2 pregnant bitches in the late stage of gestation (2.5-year-old mongrel and 3-year-old dachshund) and 10 nonpregnant bitches (6 beagles, a shibainu, a golden retriever, a basset hound, and a shih tzu, 2-10 years of age). The tissue samples excised by ovariohysterectomy were kindly provided by the dog owners at our Veterinary Teaching Hospital and the other animal hospitals close to our laboratory, and no animal was operated upon or killed specifically for this study. The corpora lutea excised from the ovary, uteri, uterine cervices and placentae were frozen in liquid nitrogen and stored at -80C for RNA extraction. For the uteri the middle portion of the uterine horn was used. In ...

ABSTRACT. This study was undertaken to develop a simple and practical method to control the time of ovulation in cynomolgus monkeys. Diets containing a synthetic gestagen, levonorgestrel (LNG) were given daily to normally cycling female monkeys for 2 weeks, and plasma concentrations of estradiol-17β and progesterone were determined by EIA in order to estimate the time of ovulation. Doses of LNG (0, 3.2,8, 20, 50, or 125 µg) were given from Day 2 (Day 0 =the first day of menstruation) through Day 15. The numbers of days from the last administration of LNG to the estimated ovulation in the groups treated with LNG at 20 µg and above were significantly greater than those in the controls, and the values in the group treated with LNG at 50 µg were within a narrow range. In a second experiment, LNG was administered at 50 µg in different phases of the menstrual cycle (16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36), and the results indicated that ovulation occurred more than 12 days after the last administration in all monkeys, and the number of days from the last administration of LNG to the estimated ovulation in the group treated on Days 16-29 (luteal phase) was significantly greater than that in the group treated on Days 23-36. These results indicate that daily provision of a diet containing 50 µg LNG could be applicable for delaying ovulation, and suggest that the total level of (exogenous and endogenous) progestins is critical for determining the length of ovulation delay in cynomolgus monkeys. KEY WORDS: control of ovulation time, levonorgestrel, monkey.doi: 10.1292/jvms.12-0023; J. Vet. Med. Sci. 74(11): 1453-1460, 2012 Monkeys, whose physiological characteristics are close to those of humans, are indispensable experimental animals. In particular, recent safety research using monkeys has contributed to the development of new drugs. Although there is much demand for monkeys as experimental animals, their reproductive efficiency is generally very low.Although estrous cycle manipulation has been used as a research and management tool for studying and maximizing reproductive performance in domestic livestock species [1,2,7], there is little information about control of the ovarian cycle in monkeys. Menstrual cycle synchronization was attempted by orally administering a progestin, altrenogest, to 4 rhesus monkeys and the possibility of achieving ovulation synchronization was suggested [8]. Daily intramuscular injection with a commonly used progestin contraceptive, levonorgestrel (LNG), inhibited follicular maturation and ovulation in cynomolgus monkeys [6]. A single subcutaneous administration of a synthetic progestogen, danazol, induced a prolonged suppression of ovarian cyclicity in cynomolgus monkeys [3]. Although these findings suggest that the use of progestogens is effective for control of ovulation in monkeys, suitable doses and effects of the treatment at different phases during the menstrual cycle had not been studied.This study was performed ...