Brain-derived neurotropic factor/TrkB signaling in the pathogenesis and novel pharmacotherapy of schizophrenia

Neurosignals. 2008;16(2-3):183-93. doi: 10.1159/000111562. Epub 2008 Feb 5.


The role of neurotropins, predominantly brain-derived neurotropic factor (BDNF), has been implicated in the pathophysiology as well as treatment outcome of schizophrenia. Both human and rodent studies indicate that the beneficial effects of antipsychotic drugs are mediated, at least in part, through BDNF and its receptor, TrkB. This review will discuss the available data on the levels of BDNF and TrkB in subjects with schizophrenia and in animals with and without conventional antipsychotics. The data concerning the impact of the antipsychotic drugs on BDNF/TrkB signaling will also be discussed. More importantly, this review will provide future perspective on BDNF/TrkB signaling as a novel molecular target to correct the pathogenesis and improve the long-term clinical outcome by treatments with conventional and adjunctive drugs.

Publication types

  • Review

MeSH terms

  • Animals
  • Antipsychotic Agents / metabolism
  • Antipsychotic Agents / pharmacology
  • Antipsychotic Agents / therapeutic use*
  • Brain-Derived Neurotrophic Factor / physiology*
  • Humans
  • Receptor, trkB / physiology*
  • Schizophrenia / drug therapy
  • Schizophrenia / etiology*
  • Schizophrenia / metabolism*
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*


  • Antipsychotic Agents
  • Brain-Derived Neurotrophic Factor
  • Receptor, trkB