Perinatal fluoxetine treatment and dams' early life stress history have opposite effects on aggressive behavior while having little impact on sexual behavior of male rat offspring.

Rationale: Many depressed women continue antidepressant treatment during pregnancy. Selective serotonin reuptake inhibitor (SSRI) treatment during pregnancy increases the risk for abnormal social development of the child, including increased aggressive or defiant behavior, with unknown effects on sexual behavior.

Objectives: Our aim was to investigate the effects of perinatal SSRI treatment and maternal depression, both separately and combined, on aggressive and sexual behavior in male rat offspring.

Perinatal fluoxetine treatment and dams' early life stress history alter affective behavior in rat offspring depending on serotonin transporter genotype and sex.

Many women diagnosed with a major depression continue or initiate antidepressant treatment during pregnancy. Both maternal stress and selective serotonin inhibitor (SSRI) antidepressant treatment during pregnancy have been associated with changes in offspring behavior, including increased anxiety and depressive-like behavior. Our aim was to investigate the effects of the SSRI fluoxetine (FLX), with and without the presence of a maternal depression, on affective behavior in male and female rat offspring.

Human progesterone receptor A and B isoforms in CHO cells. I. Stable transfection of receptor and receptor-responsive reporter genes: transcription modulation by (anti)progestagens.

A hormone-dependent transcription modulation system was established on the basis of a two-step transfection procedure of the human progesterone receptor isoforms (hPR-A and hPR-B, respectively) and a progesterone receptor-responsive reporter (MMTV-Luc). In the first step, stable transfection of the hPR-A and hPR-B isoform-encoding cDNAs was performed in the steroid receptor-negative CHO K1 cell line. Individual clones were characterized for hPR-isoform expression with respect to Western immuno-blotting, transcriptional activation and hormone binding.