Prenatal stress and early-life exposure to fluoxetine have enduring effects on anxiety and hippocampal BDNF gene expression in adult male offspring

Fabien Boulle, Jodi L. Pawluski*, Judith R. Homberg, Barbie Machiels, Yvet Kroeze, Neha Kumar, Harry W. M. Steinbusch, Gunter Kenis, Daniel L. A. Van den Hove

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


With the growing use of selective serotonin reuptake inhibitor medications (SSRIs) for the treatment of depression during the perinatal period, questions have been raised about the longterm impact of these medications on development. We aimed to investigate how developmental SSRI exposure may alter affect-related behaviors and associated molecular processes in offspring using a rodent model of maternal stress and depression. For this purpose, prenatally stressed or non-stressed male offspring were exposed to fluoxetine (5mg/kg/day) or vehicle, via lactation, until weaning. Primary results show that postnatal fluoxetine exposure differentially altered anxiety-like behavior by increasing anxiety in non-stressed offspring and decreasing anxiety in prenatally stressed offspring. In the hippocampus, developmental fluoxetine exposure decreased BDNF IV and TrkB mRNA expression. Prenatal stress alone also decreased escape behaviors and decreased hippocampal BDNF IV mRNA expression. These data provide important evidence for the long-term programming effects of early-life exposure to SSRIs on brain and behavior.
Original languageEnglish
Pages (from-to)427-438
JournalDevelopmental Psychobiology
Issue number4
Publication statusPublished - May 2016


  • SSRI
  • depression
  • prenatal stress
  • neuroplasticity
  • sex differences
  • hippocampus
  • BDNF
  • TrkB

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