3 resultados para Female sexual desire

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We investigated how queens share parentage (skew) in the Argentine ant, Linepithema humile, a social insect with multiple queens (polygyny). Overall, maternity of 546 male and female sexuals that mated successfully was determined with microsatellites in 26 colonies consisting of two queens and workers. The first main finding was that queens all contributed to sexual production. However, there was a significant departure from equal contribution to male and female sexual production in a notable proportion of colonies. Overall, reproductive skew for sexual (male and female) production was relatively low but higher than reproductive skew for egg production. The second interesting result was that there was a trade-off in the relative contribution of queens to male and female production. The queens contributing more to male production contributed significantly less to female sexual production. Finally, there was no significant association between colony productivity and the degree of reproductive skew. The relatively low reproductive skew is in line with predictions of the so-called concession models of reproductive skew because, in the Argentine ant, relatedness between queens is low and ecological constraints on dispersal nonexistent or weak. © 2001 The Association for the Study of Animal Behaviour.

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It has been shown previously that female mice homozygous for an alpha-fetoprotein (AFP) null allele are sterile as a result of anovulation, probably due to a defect in the hypothalamic-pituitary axis. Here we show that these female mice exhibit specific anomalies in the expression of numerous genes in the pituitary, including genes involved in the gonadotropin-releasing hormone pathway, which are underexpressed. In the hypothalamus, the gonadotropin-releasing hormone gene, Gnrh1, was also found to be down-regulated. However, pituitary gene expression could be normalized and fertility could be rescued by blocking prenatal estrogen synthesis using an aromatase inhibitor. These results show that AFP protects the developing female brain from the adverse effects of prenatal estrogen exposure and clarify a long-running debate on the role of this fetal protein in brain sexual differentiation.

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Two clearly opposing views exist on the function of alpha-fetoprotein (AFP), a fetal plasma protein that binds estrogens with high affinity, in the sexual differentiation of the rodent brain. AFP has been proposed to either prevent the entry of estrogens or to actively transport estrogens into the developing female brain. The availability of Afp mutant mice (Afp-/-) now finally allows us to resolve this longstanding controversy concerning the role of AFP in brain sexual differentiation, and thus to determine whether prenatal estrogens contribute to the development of the female brain. Here we show that the brain and behavior of female Afp-/- mice were masculinized and defeminized. However, when estrogen production was blocked by embryonic treatment with the aromatase inhibitor 1,4,6-androstatriene-3,17- dione, the feminine phenotype of these mice was rescued. These results clearly demonstrate that prenatal estrogens masculinize and defeminize the brain and that AFP protects the female brain from these effects of estrogens. © 2006 Nature Publishing Group.