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Sex steroids influence early organization of neural structures involved in expression of sexual behavior. A critical perinatal period during which testosterone surges occur has been identified in male rodents. Data are lacking for females, whose ovarian activity starts later in the postnatal period. Minipuberty has been described in female as a first postnatal period of gonadotropic axis activation. We transiently disrupted the minipubertal period, using daily injections of GnRH antagonist or aromatase inhibitor. The results showed unchanged puberty initiation and mild disturbance of estrus cyclicity. Minor modifications of some components of sexual behavior (olfactory preference, ability to attract male) were observed, but had no impact on lordosis behavior. Interestingly, letrozole-treated female mice showed increased anxiety state level at adulthood. This period therefore does not seem to be a key organizational window for female sexual behavior but appears to participate in the organization of neural structures involved in anxiety-related behavior. [ABSTRACT FROM AUTHOR]

Estrogen receptor (ER) α is involved in several estrogen-modulated neural and peripheral functions. To determine its role in the expression of female and male reproductive behavior, a mouse line lacking the ERα in the nervous system was generated. Mutant females did not exhibit sexual behavior despite normal olfactory preference, and had a reduced number of progesterone receptor-immunoreactive neurons in the ventromedial hypothalamus. Mutant males displayed a moderately impaired sexual behavior and unaffected fertility, despite evidences of altered organization of sexually dimorphic populations in the preoptic area. In comparison, males deleted for both neural ERα and androgen receptor (AR) displayed greater sexual deficiencies. Thus, these data highlight a predominant role for neural ERα in females and a complementary role with the AR in males in the regulation of sexual behavior, and provide a solid background for future analyses of neuronal versus glial implication of these signaling pathways in both sexes. Neural deletion of the estrogen receptor, ERα, inhibits sexual behavior in female mice, but only has moderately effect in male mice. These results contrast with previous studies using global ERα knockouts, which found that ERα is mandatory for reproductive behavior in both sexes. [ABSTRACT FROM AUTHOR]

Phthalates are organic pollutants frequently detected in the environment. The effects of these substances on male reproduction have been extensively studied but their potential impact on female reproductive behaviors in particular at environmental doses still remains to be documented. In the present study, we examined the effects of chronic exposure to di (2-ethylhexyl) phthalate (DEHP) alone at 5 or 50 μg/kg/d, or in an environmental phthalate mixture on maternal behavior of lactating female mice after a first (primiparous) and a second gestation (multiparous). Exposure of DEHP alone or in a phthalate mixture reduced pup-directed behaviors, increased self-care and forced nursing behaviors and altered nest quality for both primiparous and multiparous dams. In pup-retrieval test, primiparous and multiparous dams exposed to DEHP alone or in a phthalate mixture retrieved their pups more rapidly, probably due to a higher emission of ultrasonic vocalizations by the pups. At lactational day 2 following the third and last gestational period, the neural circuitry of maternal behavior was analyzed. A lower number of oxytocin-immunoreactive neurons in the paraventricular and anterior commissural nuclei was found in dams exposed to DEHP alone or in a phthalate mixture, while no changes were observed in the number of arginine-vasopressin immunoreactive cells. In the medial preoptic area, exposure to DEHP alone or in a phthalate mixture reduced ERα-immunoreactive cell number. Dendritic spine density assessed for DEHP at 5 μg/kg/d was also reduced. Thus, exposure to DEHP alone or in a phthalate mixture altered maternal behavior probably through a neuroendocrine mode of action involving oxytocin and estrogen through ERα, key pathways necessary for neuroplasticity and behavioral processing. [Display omitted] • Chronic exposure to environmental phthalate doses altered maternal behavior in mice. • Maternal behavior was altered in both primiparous and multiparous dams. • Offspring from phthalate-exposed dams emitted more USVs than controls. • Oxytocin-immunoreactivity was reduced in the paraventricular nucleus of phthalate-exposed dams. • ERα-immunoreactivity was reduced in the medial preoptic area of phthalate-exposed dams. [ABSTRACT FROM AUTHOR]