Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 104, Issue 11, Pages 4647-4652Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0610282104
Keywords
desipramine; electroconvulsive shock; endothelial cells; fluoxetine; neurogenesis
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Funding
- NIMH NIH HHS [MH 45481, R37 MH045481, MH 25642, P01 MH025642, R01 MH045481] Funding Source: Medline
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The neural mechanisms underlying the cellular and behavioral responses to antidepressants are not yet, known. Up-regulation of growth factors and adult neurogenesis suggest a role for one or more of these factors in the action of antidepressants. One candidate of interest is vascular endothelial growth factor (VEGF), which was initially characterized for its role in angiogenesis, but also exerts direct mitogenic effects on neural progenitors in vitro. Results of this study demonstrate that VEGF is induced by multiple classes of antidepressants at time points consistent with the induction of cell proliferation and therapeutic action of these treatments. We find that VEGF signaling through the Flk-1 receptor is required for antidepressant-induced cell proliferation. We also show that VEGF-Flk-1 signaling is required and sufficient for behavioral responses in two chronic and two subchronic antidepressant models. Taken together, these studies identify VEGF and VEGF-Flk-1 signaling as mediators of antidepressant actions and potential targets for therapeutic intervention.
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