New insights into BDNF function in depression and anxiety
Abstract
The 'neurotrophin hypothesis of depression' is based largely on correlations between stress or antidepressant treatment and down- or upregulation, respectively, of brain-derived neurotrophic factor (BDNF). Genetic disruption of the signaling pathways involving BDNF and its receptor, the tyrosine kinase TrkB, does not seem to cause depressive behaviors, but does hamper the effect of antidepressant drugs. Thus, BDNF may be a target of antidepressants, but not the sole mediator of depression or anxiety. Advances in BDNF cell biology, including its transcription through multiple promoters, trafficking and secretion, may provide new insights into its role in mood disorders. Moreover, as the precursor proBDNF and the mature protein mBDNF can elicit opposite effects on cellular functions, the impact of proBDNF and its cleavage on mood should be considered. Opposing influences of mBDNF and proBDNF on long-term potentiation and long-term depression might contribute to the dichotomy of BDNF actions on behaviors mediated by the brain stress and reward systems.
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These results lend substantial support to the neuroplasticity hypothesis of depression.
“These results lend substantial support to the neuroplasticity hypothesis of depression (sometimes referred to as the neurotrophin hypothesis) (11, 23–36).”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [29]
Favorable effects from zinc supplementation on depression-related symptoms have been demonstrated in previous clinical trials.
“favorable effects from zinc supplementation on depression-related symptoms have been demonstrated in previous clinical trials (13,51,52)”
From Effects of zinc, vitamin D, and their co-supplementation on mood, serum cortisol, and brain-derived neurotrophic factor in patients with obesity and mild to moderate depressive symptoms: A phase II, 12-wk, 2 × 2 factorial design, double-blind, randomized, placebo-controlled trial (2020) · cites this paper as [52]
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- Authors
- Martinowich, K., Manji, H., & Lu, B.
- Affiliations
- National Institutes of Health (US)
- Venue
- Nature Neuroscience
- Published
- 2007-08-28
- Volume
- 10
- Issue
- 9
- Pages
- 1089-1093
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- OpenAlex
- W1967075670
- Cited by
- 1,221
- References
- 50
- Citations by year
- 2026: 35 · 2025: 41 · 2024: 62 · 2023: 72 · 2022: 69 · 2021: 77 · 2020: 67 · 2019: 63 · 2018: 47 · 2017: 64 · 2016: 62 · 2015: 68 · 2014: 84 · 2013: 54 · 2012: 76
- FWCI
- 7.09
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- brain-derived neurotrophic factor, depression, anxiety, TrkB receptor, antidepressant mechanism, proBDNF, mature BDNF, BDNF secretion, long-term potentiation, long-term depression, stress, reward systems, mood disorders
- MeSH terms
- Animals, Antidepressive Agents, Anxiety, Depression, Humans, Signal Transduction, Brain-Derived Neurotrophic Factor
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