The
brain-derived neurotrophic factor (
BDNF) has been shown to exert an important role during implantation, placental development, and fetal growth control in mice. Its expression is closely related to the nutritional status in several tissues such as in the nervous system. In a previous study, we demonstrated that maternal
undernutrition (MU), during the perinatal life, modified both the
BDNF and its functional receptor, the
tyrosine kinase receptor B (TrkB) gene expression in the brain of growth-restricted rat offspring during sensitive developmental windows, suggesting that these early modifications may have long-lasting consequences. In the present study, we measured
BDNF/TrkB
mRNA and
protein levels in rat placentas from mothers submitted to a 50% food restriction during gestation, and in human placentas from pregnancies with
fetal growth restriction or
fetal macrosomia. In the rat, two subtypes of placental TrkB receptors have been identified: the TrkB-FL and TrkB-T1 receptors. We found that MU induced
intrauterine growth restriction (IUGR) of fetuses at term and decreased the placental
BDNF mRNA and
protein levels. Placentae from undernourished mothers exhibited an increased
mRNA expression of TrkB-FL whereas both TrkB-FL and TrkB-T1 receptors
proteins levels were not modified. In human IUGR placentas, both
BDNF and
TrkB receptor mRNA expressions were up-regulated. Finally, although neither
BDNF nor TrkB
mRNA levels were altered by
fetal macrosomia alone,
BDNF mRNA levels were decreased when macrosomia was associated with maternal
type 1 diabetes. These results show that the placental
BDNF/TrkB system is modulated in rats and humans during pregnancies with fetal growth perturbations and is affected by the maternal energetic status. These data suggest that this system may exert an important role for the feto-placental unit development and that it may also be implicated in the etiology of pathologies related to placental and fetal growth disturbances.