Variant Brain-Derived Neurotrophic Factor Val66Met Polymorphism Alters Vulnerability to Stress and Response to Antidepressants
Open accessAbstract
Brain-derived neurotrophic factor (BDNF) plays important roles in cell survival, neural plasticity, learning, and stress regulation. However, whether the recently found human BDNF Val66Met (BDNFMet) polymorphism could alter stress vulnerability remains controversial. More importantly, the molecular and structural mechanisms underlying the interaction between the BDNFMet polymorphism and stress are unclear. We found that heterozygous BDNF+/Met mice displayed hypothalamic-pituitary-adrenal axis hyperreactivity, increased depressive-like and anxiety-like behaviors, and impaired working memory compared with WT mice after 7 d restraint stress. Moreover,BDNF+/Met mice exhibited more prominent changes in BDNF levels and apical dendritic spine density in the prefrontal cortex and amygdala after stress, which correlated with the impaired working memory and elevated anxiety-like behaviors. Finally, the depressive-like behaviors in BDNF+/Met mice could be selectively rescued by acute administration of desipramine but not fluoxetine. These data indicate selective behavioral, molecular, and structural deficits resulting from the interaction between stress and the human genetic BDNFMet polymorphism. Importantly, desipramine but not fluoxetine has antidepressant effects on BDNF+/Met mice, suggesting that specific classes of antidepressant may be a more effective treatment option for depressive symptoms in humans with this genetic variant BDNF.
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Brain-derived neurotrophic factor deletion mutants are more vulnerable to stress, and targeted deletion of brain-derived neurotrophic factor in the hippocampus is sufficient to cause depressive behaviors.
“BDNF deletion mutants are also more vulnerable to stress (24, 27), and targeted deletion of BDNF in the hippocampus is sufficient to cause depressive behaviors (28).”
From Synaptic Dysfunction in Depression: Potential Therapeutic Targets (2012) · cites this paper as [27]
Different classes of antidepressants, including SSRIs, dual and triple reuptake inhibitors, dopaminergic agents, tricyclics, and ECT increase BDNF expression and the behavioral actions of these agents are blocked in BDNF deletion mutant mice.
“Different classes of antidepressants, including SSRIs, dual and triple reuptake inhibitors, dopaminergic agents, tricyclics, and ECT increase BDNF expression and the behavioral actions of these agents are blocked in BDNF deletion mutant mice135–137, 138.”
From Synaptic plasticity and depression: new insights from stress and rapid-acting antidepressants (2016) · cites this paper as [137]
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- Authors
- Yu, H., Wang, D.-D., Wang, Y., Liu, T., Lee, F. S., & Chen, Z.-Y.
- Affiliations
- Shandong University (CN)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2012-03-21
- Volume
- 32
- Issue
- 12
- Pages
- 4092-4101
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3319323
- OpenAlex
- W1996251825
- Cited by
- 275
- References
- 54
- Citations by year
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- FWCI
- 11.86
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Shandong University
- National Alliance for Research on Schizophrenia and Depression
- National Natural Science Foundation of China (31130026, 31100792, 81021001)
- China Postdoctoral Science Foundation
- National Institutes of Health (MH079513)
- Independent Innovation Foundation of Shandong University
- National Institute of Mental Health (P50MH079513, MH079513)
- National Institute of Neurological Disorders and Stroke (NS052819, R01NS052819)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- BDNF Val66Met polymorphism, brain-derived neurotrophic factor, stress vulnerability, restraint stress, depression-like behavior, anxiety-like behavior, working memory, dendritic spine density, prefrontal cortex, amygdala, desipramine, fluoxetine, antidepressant response, genetic susceptibility to depression
- MeSH terms
- Adrenocorticotropic Hormone, Analysis of Variance, Animals, Antidepressive Agents, Brain, Circadian Rhythm, Corticosterone, Corticotropin-Releasing Hormone, Depression, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Exploratory Behavior, Food Preferences, Gene Expression Regulation, Male, Methionine, Mice, Transgenic, RNA, Messenger, Stress, Psychological, Sucrose, Sweetening Agents, Swimming, Valine, Silver Staining, Pyramidal Cells, Maze Learning, Brain-Derived Neurotrophic Factor, Polymorphism, Single Nucleotide, Dendritic Spines, Serotonin Plasma Membrane Transport Proteins, Proto-Oncogene Proteins c-ets, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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