TrkB in the hippocampus and nucleus accumbens differentially modulates depression-like behavior in mice

Jochen De Vry, Tim Vanmierlo, Pilar Martinez-Martinez, Mario Losen, Yasin Temel, Janneke Boere, Gunter Kenis, Thomas Steckler, Harry W. M. Steinbusch, Marc De Baets, Jos Prickaerts*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


Brain-derived neurotrophic factor (BDNF) exerts antidepressant-like effects in the hippocampus and pro-depressant effects in the nucleus accumbens (NAc). It is thought that downstream signaling of the BDNF receptor TrkB mediates the effects of BDNF in these brain structures. Here, we evaluate how TrkB regulates affective behavior in the hippocampus and NAc. We overexpressed TrkB by electroporating a non-viral plasmid in the NAc or hippocampus in mice. Depression- and anxiety-like behaviors were evaluated in the sucrose test (anhedonia), the forced swim test (despair) and the elevated zero maze (anxiety). Targeted brain tissue was biochemically analyzed to identify molecular mechanisms responsible for the observed behavior. Overexpressing TrkB in the NAc increased the number of young neuronal cells and decreased despair and basal corticosterone levels. TrkB overexpression in the hippocampus increased astrocyte production and activation of the transcription factor CREB, yet without altering affective behavior. Our data suggest antidepressant effects of BDNF-TrkB in the NAc, which could not be explained by activation of the transcription factors CREB or beta-catenin. The effects TrkB has on depression-related behavior in different brain regions appear to critically depend on the targeted cell type.
Original languageEnglish
Pages (from-to)15-25
JournalBehavioural Brain Research
Publication statusPublished - 1 Jan 2016


  • TrkB
  • Nucleus Accumbens
  • Hippocampus
  • Depression
  • Electroporation

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