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Comparing postnatal development of gonadal hormones and associated social behaviors in rats, mice, and humans.

08:00 EDT 14th May 2018 | BioPortfolio

Summary of "Comparing postnatal development of gonadal hormones and associated social behaviors in rats, mice, and humans."

Postnatal development includes dramatic changes in gonadal hormones and the many social behaviors they help regulate, both in rodents and humans. Parental care-seeking is the most salient social interaction in neonates and infants, play and pro-social behaviors are commonly studied in juveniles, and the development of aggression and sexual behavior begins in peripubertal stages but continues through late adolescence into adulthood. While parental behaviors are shown after reproductive success in adulthood, alloparenting behaviors are actually high in juveniles as well. These behaviors are sensitive to both early life organizational effects of gonadal hormones and later life activational regulation. However, changes in circulating gonadal hormones and the display of the above behaviors over development differs between rats, mice and humans. These endpoints are of interest to endocrinologist, toxicologists, neuroscientists because of their relevance to mental health disorders and their vulnerability to effects of endocrine disrupting chemical exposure. As such, the goal of this minireview is to succinctly describe and relate the postnatal development of gonadal hormones and social behaviors to each other, over time and across animal models. Ideally, this will help identify appropriate animal models and age ranges for continued study of both normative development and in contexts of environmental disruption.

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This article was published in the following journal.

Name: Endocrinology
ISSN: 1945-7170
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Medical and Biotech [MESH] Definitions

In gonochoristic organisms, congenital conditions in which development of chromosomal, gonadal, or anatomical sex is atypical. Effects from exposure to abnormal levels of GONADAL HORMONES in the maternal environment, or disruption of the function of those hormones by ENDOCRINE DISRUPTORS are included.

Condition resulting from deficient gonadal functions, such as GAMETOGENESIS and the production of GONADAL STEROID HORMONES. It is characterized by delay in GROWTH, germ cell maturation, and development of secondary sex characteristics. Hypogonadism can be due to a deficiency of GONADOTROPINS (hypogonadotropic hypogonadism) or due to primary gonadal failure (hypergonadotropic hypogonadism).

Complete or partial change from one sex to another with regard to gonadal development. Gonadal sex reversal may occur naturally or be induced by factors such as steroids, temperature, and autosomal abnormalities during the critical period of gonadal differentiation (SEX DIFFERENTIATION) in some species.

Development of SEXUAL MATURATION in boys and girls at a chronological age that is 2.5 standard deviations below the mean age at onset of PUBERTY in the population. This early maturation of the hypothalamic-pituitary-gonadal axis results in sexual precocity, elevated serum levels of GONADOTROPINS and GONADAL STEROID HORMONES such as ESTRADIOL and TESTOSTERONE.

Hormones produced by the GONADS, including both steroid and peptide hormones. The major steroid hormones include ESTRADIOL and PROGESTERONE from the OVARY, and TESTOSTERONE from the TESTIS. The major peptide hormones include ACTIVINS and INHIBINS.

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