Stress during gestation induces strengthening inflammatory pain response and provokes development of depression. The serotoninergic system and its 5-HT1A receptors play an important role in these events. Activation of 5-HT1A receptors is known to increase the resistance of an organism to stress. During prenatal period, 5-HT1A receptors of the hippocampus and raphe nuclei are very sensitive to drugs. The aim of the present study was to test the hypothesis that injections of agonist of 5-HT1A receptors buspirone to dams before their exposure to restraint stress during the last week of pregnancy would prevent negative consequences of stress in the fetus's CNS and normalize the indices of pain- and depression-related behaviors in infant male offspring of two age groups (7-8- and 10-11-day-old rat pups). Control, prenatally non-stressed rat pups showed lower immobility at 7 days of age than at 10 days, but there were no differences in flexing+shaking behaviors between animals of different age groups. Prenatally stressed 7-8-day-old rat pups showed increase of immobility and the number of flexes+shakes in the forced swim and the formalin tests, respectively. Prenatal stress failed to alter these behaviors in 10-11-day-old animals. Daily injection of buspirone (3 mg/kg, i.p., during 9-21 days of gestation, 10 min prior to stress) normalized the behaviors in both tests in 7-8-day-olds, but profoundly decreased the indices of the behaviors (even below the control values) in 10-11-day-olds rats. The degree of manifestation of these effects depends on age of infants and is associated probably with the different level of functional activity of the serotoninergic system in the young and old age groups of the rat pups.