CoChat
Sign Up
Cited by 80Treatment of Major DepressionNeurotransmitter Receptor Influence on BehaviorTryptophan and brain disorders

Beyond the serotonin deficit hypothesis: Communicating a neuroplasticity framework of major depressive disorder

Open access
Page, Chloe E., Epperson, C. Neill, Novick, Andrew M., Duffy, Korrina A., Thompson, Scott M.·2024·Molecular Psychiatry
DOI 10.1038/s41380-024-02625-2PMC PMC11692567
Open this paper in CoChat — free accountOpen PDF

Abstract

The serotonin deficit hypothesis explanation for major depressive disorder (MDD) has persisted among clinicians and the general public alike despite insufficient supporting evidence. To combat rising mental health crises and eroding public trust in science and medicine, researchers and clinicians must be able to communicate to patients and the public an updated framework of MDD: one that is (1) accessible to a general audience, (2) accurately integrates current evidence about the efficacy of conventional serotonergic antidepressants with broader and deeper understandings of pathophysiology and treatment, and (3) capable of accommodating new evidence. In this article, we summarize a framework for the pathophysiology and treatment of MDD that is informed by clinical and preclinical research in psychiatry and neuroscience. First, we discuss how MDD can be understood as inflexibility in cognitive and emotional brain circuits that involves a persistent negativity bias. Second, we discuss how effective treatments for MDD enhance mechanisms of neuroplasticity-including via serotonergic interventions-to restore synaptic, network, and behavioral function in ways that facilitate adaptive cognitive and emotional processing. These treatments include typical monoaminergic antidepressants, novel antidepressants like ketamine and psychedelics, and psychotherapy and neuromodulation techniques. At the end of the article, we discuss this framework from the perspective of effective science communication and provide useful language and metaphors for researchers, clinicians, and other professionals discussing MDD with a general or patient audience.

Integrity signals

Registry

Crossref · 10.1038/s41380-024-02625-2

Cites

149 of 149 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 75 cited sources checked · 0 supported · 0 flagged

  • Interpretationcitation

    The effects of serotonergic antidepressants may differ in the developing brain compared with the adult brain because of differences in plasticity.

    “The developing brain is highly plastic relative to the adult brain at baseline, and the effects of serotonergic antidepressants may differ against the labile background of development versus the stable background of adulthood [106].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [106] Takesian AE, Hensch TK. Balancing plasticity/stability across brain development. Prog Brain Res. 2013;207:3–34. source

      Not checked in the free run.

  • Interpretationreasoning

    Effective treatments for major depressive disorder enhance neuroplasticity mechanisms to restore synaptic, network, and behavioral function in ways that support adaptive cognitive and emotional processing.

    “Second, we discuss how effective treatments for MDD enhance mechanisms of neuroplasticity—including via serotonergic interventions—to restore synaptic, network, and behavioral function in ways that facilitate adaptive cognitive and emotional processing.”
    Quote in the paperNot a substantial claim
  • Premisecitation

    At baseline, the developing brain shows greater plasticity than the adult brain.

    “The developing brain is highly plastic relative to the adult brain at baseline, and the effects of serotonergic antidepressants may differ against the labile background of development versus the stable background of adulthood [106].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [106] Takesian AE, Hensch TK. Balancing plasticity/stability across brain development. Prog Brain Res. 2013;207:3–34. source

      Not checked in the free run.

  • Premisecitation

    The serotonin deficit hypothesis for major depressive disorder has persisted among clinicians and the general public despite insufficient supporting evidence.

    “The serotonin deficit hypothesis explanation for major depressive disorder (MDD) has persisted among clinicians and the general public alike despite insufficient supporting evidence.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [4] Owens MJ. Selectivity of antidepressants: from the monoamine hypothesis of depression to the SSRI revolution and beyond. J Clin Psychiatry. 2004;65:5–10.

      Not checked in the free run.

    • cites [5] Miller HL, Delgado PL, Salomon RM, Berman R, Krystal JH, Heninger GR, et al. Clinical and biochemical effects of catecholamine depletion on antidepressant-induced remission of depression. Arch Gen Psychiatry. 1996;53:117–28. source

      Not checked in the free run.

  • Premisecitation

    Rodent studies show vortioxetine boosts synaptic plasticity in the hippocampus and maturation of dendritic spines.

    “In rodents, vortioxetine increases hippocampal synaptic plasticity and dendritic spine maturation [101, 102].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [101] Waller JA, Chen F, Sánchez C. Vortioxetine promotes maturation of dendritic spines in vitro: a comparative study in hippocampal cultures. Neuropharmacology. 2016;103:143–54. source

      Not checked in the free run.

    • cites [102] Dale E, Zhang H, Leiser SC, Xiao Y, Lu D, Yang CR, et al. Vortioxetine disinhibits pyramidal cell function and enhances synaptic plasticity in the rat hippocampus. J Psychopharmacol. 2014;28:891–902. source

      Not checked in the free run.

  • May combine two claims. 18
  • Classified as probably not a substantial claim. 4

  • May combine two claims.

    Premisecitation

    In humans, serotonergic antidepressants alter emotional processing within a week, or even after a single dose: people become less prone to reading ambiguous faces as negative and show stronger attention and memory for positive over negative cues.

    “For instance, serotonergic antidepressants result in acute changes in emotion processing within a week (and even after one dose) in humans, such that individuals are less likely to interpret ambiguous faces as negative and demonstrate increased attentional and memory bias for positive versus negative stimuli (reviewed by Godlewska and Harmer [36]).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [36] Godlewska BR, Harmer CJ. Cognitive neuropsychological theory of antidepressant action: a modern-day approach to depression and its treatment. Psychopharmacology. 2021;238:1265–78. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Youth MDD may more often include impulsivity or manic symptoms because of maturational differences, and these features raise suicide risk.

    “For instance, MDD in young people may be more likely to involve impulsivity and/or symptoms of mania due to differences in brain maturation, which increase the risk for suicide [104].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [104] Brent DA. Antidepressants and suicidality. Psychiatr Clin North Am. 2016;39:503–12. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Classic antidepressants that enhance serotonin transmission outperform placebos in clinical studies and are effective in up to two-thirds of patients with major depressive disorder.

    “Classic antidepressants that enhance serotonin transmission out-perform placebos in clinical studies and are effective in up to two-thirds of patients suffering from MDD [18].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [18] Rush AJ, Trivedi MH, Wisniewski SR, Nierenberg AA, Stewart JW, Warden D, et al. Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: a STAR*D report. Am J Psychiatry. 2006;163:1905–17. source

      Not checked in the free run.

  • May combine two claims.

    Interpretationreasoning

    People with depression are likely to have negative emotional biases that may lead them to think others dislike them and to avoid interacting with others.

    “For example, people struggling with depression are likely to have negative emotional biases, which might make them think that others dislike them. This might cause people with depression to avoid interacting with others.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationnone given

    Both pharmacological and non-pharmacological treatments for major depressive disorder engage multiple neuroplasticity mechanisms, and this engagement drives their therapeutic efficacy.

    “We now know that both pharmacological and non-pharmacological treatments for MDD engage multiple mechanisms of neuroplasticity, which drives their therapeutic efficacy.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Serotonin has been implicated in impulsivity.

    “Serotonin has also been implicated in impulsivity [105].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [105] Desrochers SS, Spring MG, Nautiyal KM. A role for serotonin in modulating opposing drive and brake circuits of impulsivity. Front Behav Neurosci. 2022;16:791749. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    The serotonin deficit hypothesis has been considered incorrect for at least 20 years because the evidence is insufficient.

    “However, the serotonin deficit hypothesis has been considered incorrect for at least the last 20 years due to insufficient evidence [4, 5].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [4] Owens MJ. Selectivity of antidepressants: from the monoamine hypothesis of depression to the SSRI revolution and beyond. J Clin Psychiatry. 2004;65:5–10.

      Not checked in the free run.

    • cites [5] Miller HL, Delgado PL, Salomon RM, Berman R, Krystal JH, Heninger GR, et al. Clinical and biochemical effects of catecholamine depletion on antidepressant-induced remission of depression. Arch Gen Psychiatry. 1996;53:117–28. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In mice, knocking out the 5-HT1A receptor on dentate gyrus granule cells reduces fluoxetine-induced BDNF expression and blocks proliferation of new hippocampal neurons.

    “For example, knocking out the 5-HT1A receptor on granule cells in the dentate gyrus decreases fluoxetine-induced expression of BDNF and blocks proliferation of new hippocampal neurons in mice [97].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [97] Samuels BA, Anacker C, Hu A, Levinstein MR, Pickenhagen A, Tsetsenis T, et al. 5-HT1A receptors on mature dentate gyrus granule cells are critical for the antidepressant response. Nat Neurosci. 2015;18:1616. source

      Not checked in the free run.

  • May combine two claims.

    Interpretationreasoning

    Antidepressant treatment lowers negativity bias, which can lead to better social experiences and, over time, greater willingness to engage with others.

    “After taking an antidepressant, reduced negativity bias would promote more positive social experiences, and eventually enhance motivation to engage with others.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    In clinical trials, one subanesthetic ketamine dose gives rapid symptom relief-within 24 hours-in MDD and treatment-resistant depression, but the benefit is short-lived.

    “In contrast to the slow therapeutic actions of typical antidepressants, a single subanesthetic dose of ketamine produces rapid (within 24 h of administration) symptomatic relief in MDD and treatment resistant depression in clinical trials, though the effects are transient [108].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [108] Lapidus KAB, Levitch CF, Perez AM, Brallier JW, Parides MK, Soleimani L, et al. A randomized controlled trial of intranasal ketamine in major depressive disorder. Biol Psychiatry. 2014;76:970–6. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Ketamine rapidly alters structural and functional connectivity in reward, emotion, and cognition regions, probably via glutamate-driven excitation of underactive areas.

    “Ketamine produces rapid changes in structural and functional connectivity within many regions associated with reward, emotion, and cognitive function, likely by acting on glutamate and increasing excitation in hypoactive regions of the brain, as previously reviewed [44, 111].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [44] Thompson SM. Plasticity of synapses and reward circuit function in the genesis and treatment of depression. Neuropsychopharmacology. 2023;48:90–103. source

      Not checked in the free run.

    • cites [111] Zavaliangos-Petropulu A, Al-Sharif NB, Taraku B, Leaver AM, Sahib AK, Espinoza RT, et al. Neuroimaging-derived biomarkers of the antidepressant effects of ketamine. Biol Psychiatry Cogn Neurosci Neuroimaging. 2023;8:361–86.

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    CBT helps patients process information more positively or productively, reshaping the cognitive and emotional schemas they use to interpret past and future.

    “For instance, CBT helps patients process information in positive or productive ways that change the cognitive and emotional schemas with which they understand their past and contextualize their future [153].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [153] Brewin CR. Understanding cognitive behaviour therapy: a retrieval competition account. Behav Res Ther. 2006;44:765–84. source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    Non-pharmacological depression treatments may act through mechanisms that overlap with or resemble those of standard antidepressants and psychedelics.

    “The mechanisms by which non-pharmacological treatments for depression work may be the same as or similar to those acted on by typical antidepressants and psychedelics.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Ketamine's fast and lasting antidepressant effects probably arise from different mechanisms: an initial glutamate surge sets off longer-term neuroplastic changes.

    “Distinct mechanisms of action likely underlie ketamine’s rapid versus sustained antidepressant effects, with acute increases in glutamatergic transmission triggering sustained increases in downstream processes underlying neuroplasticity, as reviewed by Kim et al. [115].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [115] Kim JW, Suzuki K, Kavalali ET, Monteggia LM. Bridging rapid and sustained antidepressant effects of ketamine. Trends Mol Med. 2023;29:P364. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In MDD, TMS raises dorsolateral PFC activation, cortico-mesolimbic connectivity, and extracellular glutamate and dopamine in the NAc.

    “TMS for MDD increases activation in the dorsolateral PFC, connectivity in cortico-mesolimbic circuitry, and extracellular glutamate and dopamine in the NAc [140, 142].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [140] Tik M, Hoffmann A, Sladky R, Tomova L, Hummer A, Navarro de Lara L, et al. Towards understanding rTMS mechanism of action: stimulation of the DLPFC causes network-specific increase in functional connectivity. Neuroimage. 2017;162:289–96. source

      Not checked in the free run.

    • cites [142] Zangen A, Hyodo K. Transcranial magnetic stimulation induces increases in extracellular levels of dopamine and glutamate in the nucleus accumbens. Neuroreport. 2002;13:2401–5. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    DBS for MDD targets the cingulate cortex or striatum (including NAc) and increases activity there and in connected anhedonia/motivation areas, plus the PFC and amygdala.

    “DBS for MDD targets the cingulate cortex or the striatum, which includes the NAc, and has been shown to enhance activity in these regions and connected areas involved in anhedonia and motivation [145, 146], as well as activity in the PFC and amygdala [139].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [145] Malone DA, Dougherty DD, Rezai AR, Carpenter LL, Friehs GM, Eskandar EN, et al. Deep brain stimulation of the ventral capsule/ventral striatum for treatment-resistant depression. Biol Psychiatry. 2009;65:267–75. source

      Not checked in the free run.

    • cites [146] Riva-Posse P, Choi KS, Holtzheimer PE, Crowell AL, Garlow SJ, Rajendra JK, et al. A connectomic approach for subcallosal cingulate deep brain stimulation surgery: prospective targeting in treatment-resistant depression. Mol Psychiatry. 2018;23:843–9. source

      Not checked in the free run.

    • cites [139] Zhu Z, Hubbard E, Guo X, Barbosa DAN, Popal AM, Cai C, et al. A connectomic analysis of deep brain stimulation for treatment-resistant depression. Brain Stimul. 2021;14:1226–33. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    The SNT TMS protocol applies intermittent theta burst stimulation to the left dorsolateral PFC and was highly effective for MDD in a 2021 trial.

    “The Stanford Neuromodulation Therapy (SNT) TMS protocol uses intermittent theta burst stimulation (iTBS) targeting the left dorsolateral PFC and was shown in a 2021 clinical trial to be highly efficacious for MDD [143].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [143] Cole EJ, Phillips AL, Bentzley BS, Stimpson KH, Nejad R, Barmak F, et al. Stanford neuromodulation therapy (SNT): a double-blind randomized controlled trial. Am J Psychiatry. 2022;179:132–41. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Like SSRIs, psychedelics may exert antidepressant effects partly by boosting serotonin transmission, which then alters gene expression, glutamate and dopamine systems, and emotion/cognition networks.

    “As with SSRIs, their enhancement of serotonergic transmission is likely relevant to their antidepressant effects through downstream changes in gene expression, indirect effects on glutamatergic and dopaminergic systems, and changes in emotional and cognitive brain networks, summarized in recent reviews [128, 129].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [128] Husain MI, Ledwos N, Fellows E, Baer J, Rosenblat JD, Blumberger DM, et al. Serotonergic psychedelics for depression: what do we know about neurobiological mechanisms of action? Front Psychiatry. 2023;13:1076459. source

      Not checked in the free run.

    • cites [129] Ling S, Ceban F, Lui LMW, Lee Y, Teopiz KM, Rodrigues NB, et al. Molecular mechanisms of psilocybin and implications for the treatment of depression. CNS Drugs. 2022;36:17–30. source

      Not checked in the free run.

    • Rests on an assumption: Psilocybin and LSD act as agonists at essentially all serotonin receptors and produce psychedelic effects by activating 5-HT2A receptors.

  • May combine two claims.

    Premisecitation

    Imaging studies indicate ketamine reduces anhedonia and boosts reward sensitivity in MDD, alongside greater activity in mesolimbic networks.

    “Neuroimaging research shows that ketamine also rescues anhedonia and enhances sensitivity to reward in patients with MDD, which is accompanied by increased activity in relevant mesolimbic brain networks [112, 113].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [112] Sterpenich V, Vidal S, Hofmeister J, Michalopoulos G, Bancila V, Warrot D, et al. Increased reactivity of the mesolimbic reward system after ketamine injection in patients with treatment-resistant major depressive disorder. Anesthesiology. 2019;130:923–35. source

      Not checked in the free run.

    • cites [113] Pulcu E, Guinea C, Cowen PJ, Murphy SE, Harmer CJ. A translational perspective on the anti-anhedonic effect of ketamine and its neural underpinnings. Mol Psychiatry. 2022;27:87. source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Reports of ketamine abuse exist in the literature.

    “Ketamine abuse has been reported in the literature, as previously reviewed [119] and was the topic of a 2020 special issue of Behavioural Brain Research [120], emphasizing the need for caution.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [119] Liu Y, Lin D, Wu B, Zhou W. Ketamine abuse potential and use disorder. Brain Res Bull. 2016;126:68–73. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Exercise and meditation can reduce depression, probably partly by boosting neurotrophic factor signaling such as BDNF.

    “Activities like physical exercise and meditation also have antidepressant effects, likely in part through enhancing signaling of neurotrophic factors like BDNF, summarized in previous reviews [154, 155].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [154] Zoladz JA, Pilc A. The effect of physical activity on the brain derived neurotrophic factor: from animal to human studies. J Physiol Pharmacol. 2010;61:533–41.

      Not checked in the free run.

    • cites [155] You T, Ogawa EF. Effects of meditation and mind-body exercise on brain-derived neurotrophic factor: a literature review of human experimental studies. Sports Med Health Sci. 2020;2:7–9. source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The FDA currently approves esketamine for depression at one or two doses weekly.

    “However, for esketamine in the treatment of depression, the current FDA approved use is once to twice per week [121], lowering risks of abuse liability in clinical settings.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [121] Janssen. SPRAVATO ® (esketamine) nasal spray, CIII Highlights of Prescribing Information. AccessdataFdaGov. 2023:1–15.

      Not checked in the free run.

22 of 22

  • The paper relies on this without support.

    Communicating an updated neuroplasticity framework to patients and the public will help combat rising mental health crises and eroding trust in science and medicine.

    “To combat rising mental health crises and eroding public trust in science and medicine, researchers and clinicians must be able to communicate to patients and the public an updated framework of MDD”

  • The paper relies on this without support.

    There are rising mental health crises and public mistrust in science and medicine.

    “Given rising mental health crises alongside public mistrust in science and medicine, we believe that effective science communication is of critical importance.”

  • The paper relies on this without support.

    Psilocybin and LSD act as agonists at essentially all serotonin receptors and produce psychedelic effects by activating 5-HT2A receptors.

    “Psilocybin and LSD are serotonergic psychedelics that act as agonists of essentially all serotonin receptors and produce their psychedelic response by activating 5-HT2A receptors.”

  • The paper relies on this without support.

    ECT causes more global brain excitation than initially targeting a single brain region.

    “In contrast, ECT causes more global excitation throughout the brain as opposed to initially targeting a single brain region.”

  • The paper relies on this without support.

    If accurate communication does not occur, the void will inevitably be filled by unintentional or intentional distortions that increase misinformation and stigma and erode public trust.

    “If we fail to do so, the risks are great: the void will inevitably be filled by unintentional or even intentional distortions that have the potential to increase misinformation and stigma while eroding public trust in science and medicine.”
5 of 5

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Computational tools that integrate fMRI and EEG already recover predictive signatures of response and can propose dose and timing schedules aligned to individual network states.

    “Computational tools that integrate fMRI and EEG already recover predictive signatures of response and can propose dose and timing schedules aligned to individual network states [14,37,181].”

    From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [37]

    The section on network-level activity reports that cortical neural variability predicts CBT efficacy in people with social anxiety. The paper does not say that computational tools integrate fMRI and EEG to predict response or propose individualized dose and timing schedules; its discussion of imaging and EEG in the non-pharmacological treatments section concerns observed brain changes, not such a tool. No page number was provided for these passages. (LLM, conf=0.79)

    Experimental — accuracy not yet measured

  • SSRIs can induce a variety of neuroplastic effects as well as changes in cognitive and emotional processing.

    “Indeed, SSRIs can induce a variety of neuroplastic effects as well as changes in cognitive and emotional processing (Page et al., 2024).”

    From Revisiting the SSRI vs. placebo debate in the treatment of social anxiety disorder: the role of expectancy effects, neural responsivity, and monoamine transporters (2025) · cites this paper as Page et al., 2024

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • A study cited for healthy participants concerns treatment-resistant depression

    Minor

    The sentence attributes the cited connectivity findings to healthy participants, but reference 134 is explicitly a study of psilocybin for treatment-resistant depression. Reference 133 may support the healthy-participant claim; reference 134 does not describe that population.

1 of 1

Cites

Flagged first, then by citations

Research works printed but not linked: 2

  1. Bartova L, Lanzenberger R, Rujescu D, Kasper S. Reply to: ‘The serotonin theory of depression: a systematic umbrella review of the evidence’ published by Moncrieff J, Cooper RE, Stockmann T, Amendola S, Hengartner MP, Horowitz MA in Molecular Psychiatry (2022 Jul 20. https://doi.org/10.1038/s41380-022-01661-0). Mol Psychiatry. 2023;28:3153–4. · DOI · Paper page
  2. Novick AM. What to say: changing the way we think about (and with) antidepressants. National Neuroscience Curriculum Initiative (NNCI); 2019. https://nncionline.org/course/what-to-say-changing-the-way-we-think-about-and-with-antidepressants/. · DOI · Paper page

Cited by

Sorted by citations

Related

Authors
Page, C. E., Epperson, C. N., Novick, A. M., Duffy, K. A., & Thompson, S. M.
Affiliations
University of Colorado Anschutz (US)
Corresponding author
Thompson, Scott M.
ORCID
Venue
Molecular Psychiatry
Publisher
Springer Science and Business Media LLC
Published
2024-05-31
Volume
29
Issue
12
Pages
3802-3813
ISSN
  • 1359-4184 (ISSN-L)
  • 1476-5578
DOI
10.1038/s41380-024-02625-2
PMC
PMC11692567
OpenAlex
W4399247518
Cited by
80
References
148
Citations by year
2026: 44 · 2025: 33 · 2024: 3
FWCI
5.01
Type
journal article
Language
en
Open access
Licence
Locations
  • Molecular Psychiatry (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Anschutz Medical Campus, University of Colorado
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (L30 HD106379, K23HD110435)
Topics
  • Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords
major depressive disorder, neuroplasticity, pathophysiology, negativity bias, cognitive inflexibility, serotonergic antidepressants, ketamine, psychedelics, neuromodulation, psychotherapy, science communication, brain circuits
MeSH terms
Antidepressive Agents, Brain, Major Depressive Disorder, Depressive Disorder, Major, Humans, Neuronal Plasticity, Serotonin

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.

Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-05.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-05.

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 ›

Are you an author, or do you see a problem with this page? Request a review