Neural correlates of change in major depressive disorder anhedonia following open-label ketamine
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Anhedonia is a cardinal symptom of major depression and is often refractory to standard treatment, yet no approved medication for this specific symptom exists. In this exploratory re-analysis, we assessed whether administration of rapid-acting antidepressant ketamine was associated specifically with reduced anhedonia in medication-free treatment-refractory patients with major depressive disorder in an open-label investigation. Additionally, participants received either oral riluzole or placebo daily beginning 4 hours post-infusion. A subgroup of patients underwent fluorodeoxyglucose positron emission tomography scans at baseline (1–3 days pre-infusion) and 2 hours post-ketamine infusion. Anhedonia rapidly decreased following a single ketamine infusion; this was sustained for up to three days, but was not altered by riluzole. Reduced anhedonia correlated with increased glucose metabolism in the hippocampus and dorsal anterior cingulate cortex (dACC) and decreased metabolism in the inferior frontal gyrus and orbitofrontal cortex (OFC). The tentative relationship between change in anhedonia and glucose metabolism remained significant in dACC and OFC, and at trend level in the hippocampus, a result not anticipated, when controlling for change in total depression score. Results, however, remain tenuous due to the lack of a placebo control for ketamine. In addition to alleviating overall depressive symptoms, ketamine could possess anti-anhedonic potential in major depressive disorder, which speculatively, may be mediated by alterations in metabolic activity in the hippocampus, dACC and OFC.
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Antidepressant effects of low-dose ketamine and transcranial magnetic stimulation can improve cerebral glucose metabolism in these regions.
“Antidepressant effects of low-dose ketamine [56] and transcranial magnetic stimulation can improve the cerebral glucose metabolism in these regions [57–60].”
From APOE4 genotype exacerbates the depression-like behavior of mice during aging through ATP decline (2021) · cites this paper as [56]
The Abstract reports that reduced anhedonia after ketamine correlated with increased glucose metabolism in the hippocampus and dACC, but with decreased metabolism in the inferior frontal gyrus and OFC. The Discussion calls the imaging findings tentative because the ketamine study lacked a placebo control. Thus the paper supports an association between ketamine response and metabolic changes in specific regions, not a general claim that ketamine improves metabolism across the regions referred to; the sentence cites other sources for transcranial magnetic stimulation. (LLM, conf=0.83)
Experimental — accuracy not yet measuredAmong patients with TRD, a single ketamine infusion rapidly reduced anhedonic symptoms, and reduction in anhedonia correlated with decreased metabolism in the right lateral OFC and increased glucose metabolism in dACC.
“First, among patients with TRD, a single ketamine infusion rapidly reduced anhedonic symptoms, and reduction in anhedonia correlated with decreased metabolism in the right lateral OFC (as well as increased glucose metabolism in dACC) [116].”
From Prefrontal cortex and depression (2022) · cites this paper as [116]
Ketamine rapidly reduces anhedonia.
“and to rapidly reduce anhedonia 25–27.”
From Mechanisms of ketamine action as an antidepressant (2018) · cites this paper as [26]
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- Authors
- Lally, N., Nugent, A. C., Luckenbaugh, D. A., Niciu, M. J., Roiser, J. P., & Zarate, C. A.
- Affiliations
- National Institutes of Health (US)
- University College London (GB)
- Corresponding author
- Lally, Níall
- Venue
- Journal of Psychopharmacology
- Publisher
- SAGE Publications
- Published
- 2015-02-17
- Volume
- 29
- Issue
- 5
- Pages
- 596-607
- ISSN
- 0269-8811 (ISSN-L)
- 1461-7285
- PMC
- PMC5116382
- OpenAlex
- W2113067674
- Cited by
- 224
- References
- 70
- Citations by year
- 2026: 6 · 2025: 13 · 2024: 32 · 2023: 20 · 2022: 33 · 2021: 27 · 2020: 18 · 2019: 22 · 2018: 15 · 2017: 12 · 2016: 19 · 2015: 7
- FWCI
- 12.63
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Psychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- National Institutes of Health
- U.S. Public Health Service (04-M-0222)
- National Institute of Mental Health (ZIAMH002857)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Health Sciences › Medicine › Psychiatry and Mental health › Electroconvulsive Therapy Studies
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- ketamine, anhedonia, major depressive disorder, treatment-resistant depression, rapid-acting antidepressants, riluzole, glucose metabolism, hippocampus, dorsal anterior cingulate cortex, orbitofrontal cortex, inferior frontal gyrus, neural correlates, FDG-PET
- MeSH terms
- Adult, Antidepressive Agents, Major Depressive Disorder, Double-Blind Method, Female, Gyrus Cinguli, Hippocampus, Humans, Ketamine, Male, Middle Aged, Radionuclide Imaging, Treatment Outcome, Anhedonia, Depressive Disorder, Treatment-Resistant
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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