Selective serotonin reuptake inhibitors (SSRIs) as fluoxetine are generally prescribed as antidepressant for depression treatment. Fluoxetine administration during pregnancy might be a risk factor for cardiorespiratory diseases in human fetus, as persistent pulmonary hypertension (Chambers et al., 2006). Serotonin (5-HT) is a neurotransmitter involved in nervous maturational processes even at the fetal stage, being an important modulator of respiratory rhythm. The serotoninergic receptors 5-HT1A and 5-HT2A are found within respiratory neurons and they play a key role in this process, beyond they are related to hypercapnia and hypoxia responses. Therefore, the goal of the present study was to evaluate the possible effects of an exposure to SSRIs during a critical period of the development, prenatal period, on respiratory control system of newborn male rats (P6). To this end, pregnant female rats received via oral gavage vehicle (apyrogenic sterile saline + 0.2% Tween-80) or fluoxetine (10mg/kg) from 15th to the 21st day of gestation and the ventilation of pups was studied. The pups were divided in control group (mother received saline during pregnancy) or SSRI group (mother received fluoxetine during pregnancy). We calculated minute ventilation (VE) of newborn male rats (P6) by using the pressure-plethysmography from the body chamber method which shows the pressure signal that we measured during breathing is directly proportional to tidal volume (VT). These measurements were made during 30 min exposure to room air followed by 30 min exposure to 7% CO2 (hypercapnia) or 30 min exposure to 10% O2 (hypoxia), then the newborns were recovered in normocapnic/normoxic conditions for 45 min and exposed to 10% O2 or 7% CO2 for 30 min. Hypercapnia exposure induced an increase in VE in the control group but did not change ventilation in the SSRI group. There were differences between groups [20 min of hypercapnia: control group: 112.95±1.31 (% of baseline); SSRI group: 104.76±3.61 (% of baseline), p<0.05, two-way ANOVA]. Hypoxia induced an increase in VE in both groups, however the ventilatory response to hypoxia was higher in SSRI group [30 min of hypoxia: control group: 128.14±13.76 (% of baseline); SSRI group: 163.91±11.72 (% of baseline), p<0.05, two-way ANOVA]. The depressor response to hypoxia in the control group is not observed in SSRI group. These preliminary results suggest that in SSRI group the CO2 chemosensitivity might be reduced whereas the O2 chemosensitivity might be increased.