ArticlePloS one2011
Antidepressant drugs transactivate TrkB neurotrophin receptors in the adult rodent brain independently of BDNF and monoamine transporter blockade.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 123 citations in OpenAlex.
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- The neurotoxicity of iodoacetic acid, a byproduct of drinking water disinfection.Frontiers in toxicology · 2025Review
- Comment on: Antidepressants act by directly binding to TRKB neurotrophin receptors.Molecular psychiatry · 2024Article
- cAMP-dependent protein kinase signaling is required for (Journal of neurophysiology · 2024Article
- The multifaceted effects of fluoxetine treatment on cognitive functions.Frontiers in pharmacology · 2024Review
- Linking Hypothermia and Altered Metabolism with TrkB Activation.ACS chemical neuroscience · 2023Article
- Receptor-Independent Anti-Ferroptotic Activity of TrkB Modulators.International journal of molecular sciences · 2022Article
- BDNF as a Mediator of Antidepressant Response: Recent Advances and Lifestyle Interactions.International journal of molecular sciences · 2022Review
- Mechanisms of ketamine and its metabolites as antidepressants.Biochemical pharmacology · 2022Review
- Antidepressant-like Effects of BDNF and NGF Individual Loop Dipeptide Mimetics Depend on the Signal Transmission Patterns Associated with Trk.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Pharmacogenetic inhibition of TrkB signaling in adult mice attenuates mechanical hypersensitivity and improves locomotor function after spinal cord injury.Frontiers in cellular neuroscience · 2022Article
- Analysis of Antidepressant-like Effects and Action Mechanisms of GSB-106, a Small Molecule, Affecting the TrkB Signaling.International journal of molecular sciences · 2021Article
- Facilitation of TRKB Activation by the Angiotensin II Receptor Type-2 (AT2R) Agonist C21.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Review
- Dysregulated copper transport in multiple sclerosis may cause demyelination via astrocytes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Transient Stimulation with Psychoplastogens Is Sufficient to Initiate Neuronal Growth.ACS pharmacology & translational science · 2021Article
- Ketamine-50 years in use: from anesthesia to rapid antidepressant effects and neurobiological mechanisms.Pharmacological reports : PR · 2021Review
- Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAntidepressant drugs (ADs) have been shown to activate BDNF (brain-derived neurotrophic factor) receptor TrkB in the rodent brain but the mechanism underlying this phenomenon remains unclear. ADs act as monoamine reuptake inhibitors and after prolonged treatments regulate brain bdnf mRNA levels indicating that monoamine-BDNF signaling regulate AD-induced TrkB activation in vivo. However, recent findings demonstrate that Trk receptors can be transactivated independently of their neurotrophin ligands. METHODOLOGY: In this study we examined the role of BDNF, TrkB kinase activity and monoamine reuptake in the AD-induced TrkB activation in vivo and in vitro by employing several transgenic mouse models, cultured neurons and TrkB-expressing cell lines. PRINCIPAL
findingsUsing a chemical-genetic TrkB(F616A) mutant and TrkB overexpressing mice, we demonstrate that ADs specifically activate both the maturely and immaturely glycosylated forms of TrkB receptors in the brain in a TrkB kinase dependent manner. However, the tricyclic AD imipramine readily induced the phosphorylation of TrkB receptors in conditional bdnf⁻/⁻ knock-out mice (132.4±8.5% of control; P = 0.01), indicating that BDNF is not required for the TrkB activation. Moreover, using serotonin transporter (SERT) deficient mice and chemical lesions of monoaminergic neurons we show that neither a functional SERT nor monoamines are required for the TrkB phosphorylation response induced by the serotonin selective reuptake inhibitors fluoxetine or citalopram, or norepinephrine selective reuptake inhibitor reboxetine. However, neither ADs nor monoamine transmitters activated TrkB in cultured neurons or cell lines expressing TrkB receptors, arguing that ADs do not directly bind to TrkB.
conclusionsThe present findings suggest that ADs transactivate brain TrkB receptors independently of BDNF and monoamine reuptake blockade and emphasize the need of an intact tissue context for the ability of ADs to induce TrkB activity in brain.
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