Perinatal exposure to fluoxetine via placenta and lactation inhibits the testicular development in male rat offspring.

Due to the widespread use of fluoxetine to treat depression, including pregnant and nursing women, the present study aimed to investigate the effects of in utero and lactational exposure to fluoxetine in rat offspring at post natal day 22. Wistar rat dams were orally treated with fluoxetine (5, 10, and 20 mg/kg) from day 13 gestation to day 21 lactation. Exposure to 10 and 20 mg/kg fluoxetine reduced the body and testis weights. The volume of the seminiferous tubules and epithelium were also reduced following 20 mg/kg fluoxetine exposure. The length of the seminiferous tubules and the population of Sertoli cells changed in offspring exposed to fluoxetine. The amount of seminiferous tubules lacking tubular lumen was higher in rats exposed to 20 mg/kg fluoxetine. Plasma testosterone showed no significant change. In conclusion, fluoxetine exposure via the placenta and lactation may inhibit and delay testicular development, adversely affecting several testicular parameters important for the establishment of sperm production in adulthood.

Exposure of developing well-nourished and malnourished rats to environmental heating facilitates cortical spreading depression propagation at adulthood.

Cortical spreading depression (CSD) is a brain electrical response related to neural activity and probably also related to diseases like migraine and epilepsy. Adverse conditions like malnutrition and exposure to a warm environment early-in-life can permanently alter brain development, changing electrophysiological features of the brain responses and rendering the brain prone to febrile seizures. Here we investigated the lasting effects of heat exposure on brain CSD propagation in well-nourished and malnourished developing rats. From postnatal days 10-29, rats were exposed to daily sessions (one session per day, five sessions per week during 3 weeks; total of 15 sessions) of a warm environment (40+/-2 degrees C). At 30-40 days and 90-120 days of life (young and adult age-ranges, respectively), they were anesthetized (urethane+chloralose; 1000 + 40 mg/kg ip) and the electrocorticogram plus the slow potential change accompanying CSD were recorded on two parietal points for 4h. Compared to controls (maintained on the normal environment temperature, 23+/-2 degrees C), heat-exposed rats displayed higher CSD velocities of propagation (P<0.05; ANOVA plus Tukey test) at both age-ranges and nutritional statuses. The mean+/-S.D. CSD velocities (in mm/min) were: for control- and heat-exposed well-nourished rats, 3.75+/-0.15 and 4.17+/-0.19 (young groups), and 3.33+/-0.06 and 3.88+/-0.26 (adult); for the same control and heat exposure conditions in the malnourished rats, 4.30+/-0.22 and 5.31+/-0.46 (young), and 4.18+/-0.20 and 4.88+/-0.35 (adult). In contrast to early malnutrition, heat exposure did not affect body and brain weights. Data support the hypotheses that (1) early heat exposure long-lasting facilitates CSD propagation and (2) this effect is not modified by early malnutrition.