BDNF Val66Met impairs fluoxetine-induced enhancement of adult hippocampus plasticity
Open accessAbstract
Recently, a single-nucleotide polymorphism (SNP) in the brain-derived neurotrophic factor (BDNF) gene (BDNF Val66Met) has been linked to the development of multiple forms of neuropsychiatric illness. This SNP, when genetically introduced into mice, recapitulates core phenotypes identified in human BDNF Val66Met carriers. In mice, this SNP also leads to elevated expression of anxiety-like behaviors that are not rescued with the prototypic selective serotonin reuptake inhibitor (SSRI), fluoxetine. A prominent hypothesis is that SSRI-induced augmentation of BDNF protein expression and the beneficial trophic effects of BDNF on neural plasticity are critical components for drug response. Thus, these mice represent a potential model to study the biological mechanism underlying treatment-resistant forms of affective disorders. To test whether the BDNF Val66Met SNP alters SSRI-induced changes in neural plasticity, we used wild-type (BDNF(Val/Val)) mice, and mice homozygous for the BDNF Val66Met SNP (BDNF(Met/Met)). We assessed hippocampal BDNF protein levels, survival rates of adult born cells, and synaptic plasticity (long-term potentiation, LTP) in the dentate gyrus either with or without chronic (28-day) fluoxetine treatment. BDNF(Met/Met) mice had decreased basal BDNF protein levels in the hippocampus that did not significantly increase following fluoxetine treatment. BDNF(Met/Met) mice had impaired survival of newly born cells and LTP in the dentate gyrus; the LTP effects remained blunted following fluoxetine treatment. The observed effects of the BDNF Val66Met SNP on hippocampal BDNF expression and synaptic plasticity provide a possible mechanistic basis by which this common BDNF SNP may impair efficacy of SSRI drug treatment.
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BDNFmet/met mice show decreased fluoxetine efficacy through impaired synaptic plasticity, including reduced theta-burst stimulation-induced LTP, impaired survival of newborn hippocampal cells, and a deficit in PFC synaptic transmission.
“subsequent experiments showed that this genetic variant decreased fluoxetine efficacy through impaired synaptic plasticity defined by a reduction of theta-burst stimulation-induced LTP as well as impairments in the survival of newborn cells in the hippocampus (Bath et al. 2012; Ninan et al. 2010) and a deficit in synaptic transmission in the PFC (Pattwell et al. 2012).”
From Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression (2018) · cites this paper as Bath et al. 2012
The dentate-gyrus Results report reduced LTP in BDNF Met/Met mice that fluoxetine did not significantly improve, and the Discussion reports fewer surviving newborn hippocampal cells. But the Methods specify 100 Hz stimulation, not theta-burst stimulation; the Discussion also says fluoxetine increased newborn-cell survival. The citing sentence attributes the separate PFC finding to Pattwell et al., not to this paper. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe effects of the traditional antidepressant fluoxetine on synaptic plasticity and fear extinction are dependent on BDNF.
“the effects of the traditional antidepressant fluoxetine on synaptic plasticity and fear extinction have been shown to be dependent on BDNF (141, 142)”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [142]
The Results section, “BDNF Met/Met Impairs Synaptic Plasticity Within the Dentate Gyrus” (page unavailable), reports that fluoxetine enhanced long-lasting potentiation in BDNF Val/Val mice but not BDNF Met/Met mice. This supports a role for BDNF genotype in fluoxetine’s effect on synaptic plasticity. Our copy does not report a test of fluoxetine’s effect on fear extinction, so that part of the claim is unsupported. (LLM, conf=0.87)
Experimental — accuracy not yet measuredTypical antidepressants, with chronic treatment, produce a slow increase in neurotrophic factor expression and enhance synaptic plasticity.
“In contrast to the effects of stress and depression, typical antidepressants, with chronic treatment, produce a slow increase in neurotrophic factor expression and enhance synaptic plasticity.”
From Synaptic Dysfunction in Depression: Potential Therapeutic Targets (2012) · cites this paper as [41]
The Introduction says nearly all antidepressant regimens tested in rodents increase hippocampal BDNF, and the results report increased BDNF and enhanced long-term potentiation after 28 days of fluoxetine in wild-type mice. The paper does not establish that the increase is slow, and these findings do not extend to the BDNF Met/Met mice studied. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIn mice with the BDNF met/met allele, SSRI-induced enhancement of BDNF levels and synaptic plasticity was impaired.
“In mice with the BDNF met/met allele SSRI-induced enhancement of BDNF levels and synaptic plasticity was impaired (Bath et al., 2012) suggesting that the lack of response to SSRIs may be tied to the observed deficits in synaptic plasticity.”
From BDNF - a key transducer of antidepressant effects (2016) · cites this paper as Bath et al., 2012
The lack of response to SSRIs may be tied to the observed deficits in synaptic plasticity.
“In mice with the BDNF met/met allele SSRI-induced enhancement of BDNF levels and synaptic plasticity was impaired (Bath et al., 2012) suggesting that the lack of response to SSRIs may be tied to the observed deficits in synaptic plasticity.”
From BDNF - a key transducer of antidepressant effects (2016) · cites this paper as Bath et al., 2012
Selective serotonin reuptake inhibitors increased long-term potentiation and synaptic transmission.
“For example, a previous study showed that selective serotonin reuptake inhibitors increased long-term potentiation (LTP), a type of heterosynaptic plasticity that is likely involved in learning and memory, as well as synaptic transmission.”
From Epigenetic mechanisms of major depression: Targeting neuronal plasticity (2018) · cites this paper as [46]
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- Authors
- Bath, K. G., Jing, D. Q., Dincheva, I., Neeb, C. C., Pattwell, S. S., Chao, M. V., Lee, F. S., & Ninan, I.
- Affiliations
- Cornell University (US)
- Weill Cornell Medicine (US)
- New York University (US)
- NYU Langone Health (US)
- Corresponding author
- Bath, Kevin G
- Lee, Francis S
- Ninan, Ipe
- Venue
- Neuropsychopharmacology
- Published
- 2012-01-04
- Volume
- 37
- Issue
- 5
- Pages
- 1297-1304
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC3306891
- OpenAlex
- W2103587403
- Cited by
- 169
- References
- 50
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 9 · 2023: 7 · 2022: 10 · 2021: 8 · 2020: 13 · 2019: 14 · 2018: 13 · 2017: 13 · 2016: 10 · 2015: 21 · 2014: 19 · 2013: 17 · 2012: 7
- FWCI
- 8.44
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neuropsychopharmacology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- New York Community Trust
- International Mental Health Research Organization
- National Alliance for Research on Schizophrenia and Depression
- Monique Weill-Caulier Trust
- National Institutes of Health (NS-21072)
- National Institute on Aging (R01AG025970)
- National Institute of Mental Health (R25MH060478, MH060478, RC1MH088814, MH088814)
- National Institute of Neurological Disorders and Stroke (R01NS021072, NS-21072, NS052819, R01NS052819, R56NS021072)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD055177, T32HD055177)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- BDNF Val66Met polymorphism, brain-derived neurotrophic factor, fluoxetine, selective serotonin reuptake inhibitors, hippocampal plasticity, synaptic plasticity, long-term potentiation, dentate gyrus, adult neurogenesis, treatment-resistant depression, single nucleotide polymorphisms, anxiety-like behavior, mood disorders
- MeSH terms
- Analysis of Variance, Animals, Biophysics, Bromodeoxyuridine, Electric Stimulation, Enzyme-Linked Immunosorbent Assay, Fluoxetine, Gene Expression Regulation, Glial Fibrillary Acidic Protein, Humans, Male, Methionine, Mice, Inbred C57BL, Mice, Transgenic, Valine, Selective Serotonin Reuptake Inhibitors, Long-Term Potentiation, Patch-Clamp Techniques, Dentate Gyrus, Brain-Derived Neurotrophic Factor, Polymorphism, Single Nucleotide, Receptor, trkB, Mice, In Vitro Techniques
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