Brain-Derived Neurotrophic Factor Val66Met Allele Impairs Basal and Ketamine-Stimulated Synaptogenesis in Prefrontal Cortex
Open accessAbstract
Background Knock-in mice with the common human brain-derived neurotrophic factor (BDNF) Val66Met polymorphism have impaired trafficking of BDNF messenger RNA to dendrites. It was hypothesized, given evidence that local synapse formation is dependent on dendritic translation of BDNF messenger RNA, that loss-of-function Met allele mice would show synaptic deficits both at baseline and in response to ketamine, an N-methyl-D-aspartate antagonist that stimulates synaptogenesis in prefrontal cortex (PFC).Methods Whole-cell recordings from layer V medial PFC pyramidal cells in brain slices were combined with two-photon laser scanning for analysis of wildtype, Val/Met, and Met/Met mice both at baseline and in response to a low dose of ketamine.Results Val/Met and Met/Met mice were found to have constitutive atrophy of distal apical dendrites and decrements in apically targeted excitatory postsynaptic currents in layer V pyramidal cells of PFC. In addition, spine density and diameter were decreased, indicative of impaired synaptic formation/maturation (synaptogenesis). In Met/Met mice the synaptogenic effect of ketamine was markedly impaired, consistent with the idea that synaptogenesis is dependent on dendritic translation/release of BDNF. In parallel behavioral studies, we found that the antidepressant response to ketamine in the forced swim test was blocked in Met/Met mice.Conclusions The results demonstrate that expression of the BDNF Met allele in mice results in basal synaptic deficits and blocks synaptogenic and antidepressant actions of ketamine in PFC, suggesting that the therapeutic response to this drug might be attenuated or blocked in depressed patients who carry the loss of function Met allele.
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The effects of ketamine at 10 mg/kg intraperitoneally on spine morphology 24 hours after treatment-increased spine number, increased diameter, and reduced length-were significantly blunted but not completely abolished in Met/Met mice.
“The effects of ketamine (10 mg/kg i.p.) on spine morphology 24 hours post-treatment, including increased spine number, increased diameter, and reduced length were significantly blunted but not completely abolished in Met/Met mice.”
From Mechanisms of ketamine and its metabolites as antidepressants (2022) · cites this paper as Liu et al., 2012
The Results section reports that, 24 hours after 10 mg/kg i.p. ketamine, spine density and head diameter increased in Val/Val mice but not overall in Met/Met mice. It also reports a small diameter increase in a subset of Met/Met spines, supporting 'blunted but not completely abolished.' The copy describes increased spine length as a baseline feature of Met/Met mice, not a ketamine-induced reduction in length. (LLM, conf=0.88)
Experimental — accuracy not yet measuredCompared with Val/Val wild-type controls, heterozygous and homozygous Val/Met and Met/Met mice showed significantly reduced dendrite length, lower distal spine density, smaller spine diameter, and greater spine length in layer 5 mPFC pyramidal neurons, with spine length unaffected in heterozygotes.
“heterozygous and homozygous Val/Met and Met/Met mice had significantly reduced dendrite length, distal spine density, reduced spine diameter, and increased spine length (spine length not impacted in heterozygotes) in layer 5 mPFC pyramidal neurons relative to Val/Val WT controls (Liu et al., 2012).”
From Mechanisms of ketamine and its metabolites as antidepressants (2022) · cites this paper as Liu et al., 2012
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredThe BDNF Val66Met single-nucleotide polymorphism causes major structural atrophy and functional deficits in the PFC and blocks the synaptogenic effects of ketamine.
“The BDNF Val66Met single-nucleotide polymorphism causes major structural atrophy and functional deficits in the PFC and blocks the synaptogenic effects of ketamine (136, 137).”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [136]
The Abstract Results and Discussion report atrophy of distal apical dendrites and reduced excitatory responses in the PFC of Val/Met and Met/Met mice. The Results section on ketamine-induced synaptogenesis says its effects in Met/Met mice were markedly impaired but “not totally blocked.” The claim overstates both the scope of the observed atrophy and the completeness of the ketamine blockade. (LLM, conf=0.90)
Experimental — accuracy not yet measuredThough the primary molecular targets of ketamine and serotonergic psychedelics are distinct, their downstream pharmacology overlaps, requiring AMPA receptor, TrkB, and mTOR activation to elicit changes in neuronal structure and function.
“Though the primary molecular targets of ketamine and serotonergic psychedelics are distinct, their downstream pharmacology overlaps, requiring AMPA receptor, TrkB, and mTOR activation to elicit changes in neuronal structure and function (135–137, 148, 153, 154).”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [136]
The Discussion (BDNF dependence of ketamine-induced rapid synaptogenesis; page not provided) describes an AMPA receptor–BDNF/TrkB–mTOR pathway leading to ketamine-induced synaptogenesis. The paper does not establish that serotonergic psychedelics require the same pathway or that their downstream pharmacology overlaps with ketamine’s. (LLM, conf=0.87)
Experimental — accuracy not yet measuredMice with the Val66Met polymorphism are insensitive to antidepressants.
“In addition, mice with Val66Met polymorphism are insensitive to antidepressants [226].”
From Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer (2020) · cites this paper as [226]
The Abstract Results report that ketamine’s antidepressant response in the forced swim test was blocked in Met/Met mice. The claim extends that finding to antidepressants generally and to mice with the polymorphism without specifying genotype. The Discussion’s Clinical implications section notes that studies of standard antidepressants do not show an overall negative effect of the Met allele on treatment outcome. (LLM, conf=0.90)
Experimental — accuracy not yet measured
The antidepressant-like effect of ketamine in the forced swim test, measured as reduced immobility, was absent in Met/Met mice.
“the antidepressant-like effects of ketamine in the forced swim test (reduced immobility) were absent in Met/Met mice.”
From Mechanisms of ketamine and its metabolites as antidepressants (2022) · cites this paper as Liu et al., 2012
Ketamine increases BDNF protein translation, and its antidepressant effects are absent when administered to inducible BDNF knockout mice or homozygous mice harboring the BDNF Val66Met mutation.
“Ketamine increases BDNF protein translation (135, 145) and its antidepressant effects are absent when administered to inducible BDNF knockout mice (135) or homozygous mice harboring the BDNF Val66Met mutation (136).”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [136]
In BDNF Val66Met knock-in mice and conditional BDNF knockout models, the antidepressant effects of ketamine are significantly reduced.
“studies using BDNF Val66Met knock-in mice and conditional BDNF knockout models in which the antidepressant effects of ketamine are significantly reduced [60,74]”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [74]
Transgenic mice carrying mutant BDNF that cannot translocate to dendrites do not display ketamine-dependent synaptogenesis nor antidepressant-like behavioral responses.
“The mTOR activation of BDNF and synaptogenesis in PFC appear to be involved in Ketamine’s therapeutic function, because transgenic mice carrying a mutant form of BDNF that cannot translocate to dendrites do not display ketamine-dependent synaptogenesis nor antidepressant-like behavioral responses 228.”
From Mechanisms of synaptic transmission dysregulation in the prefrontal cortex: pathophysiological implications (2022) · cites this paper as [228]
mTOR activation of BDNF and synaptogenesis in PFC appear involved in ketamine's therapeutic function.
“The mTOR activation of BDNF and synaptogenesis in PFC appear to be involved in Ketamine’s therapeutic function, because transgenic mice carrying a mutant form of BDNF that cannot translocate to dendrites do not display ketamine-dependent synaptogenesis nor antidepressant-like behavioral responses 228.”
From Mechanisms of synaptic transmission dysregulation in the prefrontal cortex: pathophysiological implications (2022) · cites this paper as [228]
Mice with a Val66Met single-nucleotide polymorphism in the BDNF gene exhibit impairments in BDNF release and mRNA trafficking; ketamine administration reduced synaptogenesis in the PFC and impaired antidepressant behavioral effects in these animals.
“Mice with a Val66Met single-nucleotide polymorphism in the BDNF gene exhibit impairments in BDNF release and mRNA trafficking; ketamine administration was demonstrated to have reduced synaptogenesis in the PFC and impaired antidepressant behavioral effects in these animals.107”
From Ketamine as an antidepressant: Overview of its mechanisms of action and potential predictive biomarkers (2020) · cites this paper as [107]
The blockade of NV-5138 antidepressant actions was observed in both Val/Met and Met/Met knockin mice.
“This was observed in both Val/ Met and Met/Met knockin mice, similar to complete blockade of the antidepressant actions of ketamine and scopolamine in Met/ Met mice, and partial or complete block, respectively, in Val/Met mice (37, 38).”
From Sestrin modulator NV-5138 produces rapid antidepressant effects via direct mTORC1 activation (2019) · cites this paper as [37]
Ketamine and scopolamine antidepressant actions are completely blocked in Met/Met mice and partially or completely blocked in Val/Met mice.
“This was observed in both Val/ Met and Met/Met knockin mice, similar to complete blockade of the antidepressant actions of ketamine and scopolamine in Met/ Met mice, and partial or complete block, respectively, in Val/Met mice (37, 38).”
From Sestrin modulator NV-5138 produces rapid antidepressant effects via direct mTORC1 activation (2019) · cites this paper as [37]
The Val66Met allele, found in approximately 25 percent of the population, blocks the processing and release of mature BDNF and is sufficient to cause atrophy of neurons in the hippocampal and mPFC of mice with this allele.
“Studies of a human BDNF polymorphism, Val66Met found in approximately 25 percent of the population have been insightful. The Val66Met allele, which blocks the processing and release of mature BDNF, is sufficient to cause atrophy of neurons in the hippocampal37 and mPFC of mice with this allele38.”
From Synaptic plasticity and depression: new insights from stress and rapid-acting antidepressants (2016) · cites this paper as [38]
Ketamine-induction of antidepressant behavioral responses are blocked in BDNF null mice.
“This possibility is supported by recent reports that ketamine-induction of antidepressant behavioral responses are blocked in BDNF null mice164,165.”
From Synaptic plasticity and depression: new insights from stress and rapid-acting antidepressants (2016) · cites this paper as [165]
BDNF signaling is necessary for ketamine's antidepressant actions.
“BNDF signaling was shown to be necessary for ketamine’s antidepressant actions.”
From Mechanisms of ketamine action as an antidepressant (2018) · cites this paper as [163]
Mice expressing the human BDNFVal66met (rs6265) single nucleotide polymorphism, especially Met/Met carriers, do not manifest ketamine-induced antidepressant effects.
“In support of this, mice expressing the human BDNFVal66met (rs6265) single nucleotide polymorphism (SNP) – especially Met/Met carriers –, which induces deficits in BDNF processing and activity-dependent secretion 162, do not manifest ketamine-induced antidepressant effects 163.”
From Mechanisms of ketamine action as an antidepressant (2018) · cites this paper as [163]
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- Authors
- Liu, R.-J., Lee, F. S., Li, X.-Y., Bambico, F., Duman, R. S., & Aghajanian, G. K.
- Affiliations
- Yale University (US)
- Cornell University (US)
- Corresponding author
- Aghajanian, George K.
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2012-06
- Volume
- 71
- Issue
- 11
- Pages
- 996-1005
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC3290730
- OpenAlex
- W2094166526
- Cited by
- 403
- References
- 60
- Citations by year
- 2026: 11 · 2025: 25 · 2024: 10 · 2023: 25 · 2022: 23 · 2021: 38 · 2020: 33 · 2019: 36 · 2018: 37 · 2017: 25 · 2016: 33 · 2015: 33 · 2014: 23 · 2013: 31 · 2012: 18
- FWCI
- 17.10
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (MH 17871, MH093897, R01MH093897, R37MH017871, R01MH017871)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Keywords
- brain-derived neurotrophic factor, BDNF Val66Met polymorphism, ketamine, synaptogenesis, prefrontal cortex, dendritic translation, dendritic atrophy, dendritic spines, excitatory postsynaptic currents, antidepressant response, depression, layer 5 pyramidal neurons, forced swim test
- MeSH terms
- Alleles, Animals, Dendrites, Major Depressive Disorder, Ketamine, Mice, Transgenic, Polymorphism, Genetic, RNA, Messenger, Synapses, Receptors, N-Methyl-D-Aspartate, Prefrontal Cortex, Pyramidal Cells, Patch-Clamp Techniques, Excitatory Amino Acid Antagonists, Brain-Derived Neurotrophic Factor, Excitatory Postsynaptic Potentials, Mice
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