Activation of the TrkB Neurotrophin Receptor Is Induced by Antidepressant Drugs and Is Required for Antidepressant-Induced Behavioral Effects

By Tommi Saarelainen, P. Hendolin, Guilherme Lucas, Eija Koponen, Mikko Sairanen, E. Macdonald, K. Agerman, A. Haapasalo, H. Nawa, R. Aloyz and 2 more. Journal of Neuroscience, 2003

788 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience

View Paper: https://www.semanticscholar.org/paper/bfb30f43a5cf7080541147d2d79b34698f35fdcf

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In Cellular and Molecular Neuroscience

In Developmental Neuroscience

Citations in the corpus

TrkB regulates hippocampal neurogenesis and governs sensitivity to antidepressive treatment (2008, background): “Previous studies with BDNF mutants regarding these anxiety- and depression-like behaviors have yielded mixed results: some were normal (Gorski et al., 2003; Monteggia et al., 2004; Saarelainen et al., 2003) while others were not (Chen et al., 2006; Monteggia et al., 2007; Rios et al., 2001).”
Brain-Derived Neurotrophic Factor and Neuropsychiatric Disorders (2012, background): “Although many growth factors such as NGF and insulin growth factor are also known to increase after antidepressant treatment and to cause behavioral effects similar to those observed after BDNF infusion (for review, see Duman and Monteggia, 2006), a preponderance of data suggests that animal models ”
Interaction between BDNF and Serotonin: Role in Mood Disorders (2008, background): “Thus, the rapid effects of antidepressants on FST/TST are likely mediated by an acute increase in BDNF secretion and/or TrkB signaling (Saarelainen et al, 2003), rather than by an enhancement of BDNF/TrkB gene expression.”
The role of BDNF and its receptors in depression and antidepressant drug action: Reactivation of developmental plasticity (2010, background): “Conversely, in mice with reduced brain BDNF levels or TrkB signaling, antidepressant drugs fail to produce behavioral responses (Saarelainen et al., 2003; Monteggia et al., 2004).”
Hippocampal neurogenesis: Opposing effects of stress and antidepressant treatment (2006, neutral): “(Sheline et al., 1996; Shah et al., 1998; Sheline et al., 1999; Bremner et al., 2000; Mervaala et al., 2000; Steffens et al., 2000; Frodl et al., 2002; MacQueen et al., 2003; Saarelainen et al., 2003; Sheline et al., 2003; Vermetten et al., 2003).”
The role of neurotrophic factors in adult hippocampal neurogenesis, antidepressant treatments and animal models of depressive-like behavior (2007, background): “decrease in hippocampal volume (approximately 9% on average across all studies) in patients with MDD (Sheline et al., 1996, 1998, 1999, 2003; Shah et al., 1998; Bremner et al., 2000; Mervaala et al., 2000; Steffens et al., 2000; Frodl et al., 2002; MacQueen et al., 2003; Saarelainen et al., 2003; Ve”
The chronic mild stress (CMS) model of depression: History, evaluation and usage (2016, background): “Neuronal growth is promoted by BDNF and other neurotrophins and behavioural responses to chronic antidepressant treatment (in other experimental models) are blocked in mutant mice with full or forebrainspecific impairment of either BDNF or its receptor, TrkB (Saarelainen et al., 2003; Monteggia et a”
BDNF — a key transducer of antidepressant effects (2015, background): “…of BDNF signaling in the response to antidepressants has come from studies examining the high affinity BDNF receptor, TrkB. Antidepressant drugs require functional TrkB receptors to mediate antidepressant-like response in preclinical models (Rantamäki et al., 2007; Saarelainen et al., 2003).”