The effects of low‐dose ketamine on the prefrontal cortex and amygdala in treatment‐resistant depression: A randomized controlled study

Li, Cheng‐Ta; Chen, Mu‐Hong; Lin, Wei‐Chen; Hong, Chen‐Jee; Yang, Bang‐Hung; Liu, Ren‐Shyan; Tu, Pei‐Chi; Su, Tung‐Ping

doi:10.1002/hbm.23085

Cited by 153Treatment of Major DepressionElectroconvulsive Therapy StudiesTryptophan and brain disorders

The effects of low‐dose ketamine on the prefrontal cortex and amygdala in treatment‐resistant depression: A randomized controlled study

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Li, Cheng‐Ta, Chen, Mu‐Hong, Lin, Wei‐Chen, Hong, Chen‐Jee, Yang, Bang‐Hung, Liu, Ren‐Shyan, Tu, Pei‐Chi, Su, Tung‐Ping·2016·Human Brain Mapping

DOI 10.1002/hbm.23085PMC PMC6867460

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Abstract

Background: Low‐dose ketamine has been found to have robust and rapid antidepressant effects. A hypoactive prefrontal cortex (PFC) and a hyperactive amygdala have been suggested to be associated with treatment‐resistant depression (TRD). However, it is unclear whether the rapid antidepressant mechanisms of ketamine on TRD involve changes in glutamatergic neurotransmission in the PFC and the amygdala. Methods: A group of 48 TRD patients were recruited and equally randomized into three groups (A: 0.5 kg/mg‐ketamine; B: 0.2 kg/mg‐ketamine; and C: normal saline [NS]). Standardized uptake values (SUV) of glucose metabolism measured by 18 F‐FDG positron‐emission‐tomography before and immediately after a 40‐min ketamine or NS infusion were used for subsequent region‐of‐interest (ROI) analyses (a priori regions: PFC and amygdala) and whole‐brain voxel‐wise analyses and were correlated with antidepressant responses, as defined by the Hamilton depression rating scale score. The 18 F‐FDG signals were used as a proxy measure of glutamate neurotransmission. Results: The ROI analysis indicated that Group A and Group B, but not Group C, had increases in the SUV of the PFC (group‐by‐time interaction: F = 7.373, P = 0.002), whereas decreases in the SUV of the amygdala were observed in all three groups (main effect of time, P < 0.001). The voxel‐wise analysis further confirmed a significant group effect on the PFC (corrected for family‐wise errors, P < 0.05; post hoc analysis: Group A<Group C, Group B<Group C). The SUV differences in the PFC predicted the antidepressant responses at 40 and 240 min post‐treatment. The PFC changes did not differ between those with and without side effects. Conclusion: Ketamine's rapid antidepressant effects involved the facilitation of glutamatergic neurotransmission in the PFC. Hum Brain Mapp 37:1080–1090, 2016. © 2016 Wiley Periodicals, Inc.

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Convergent data show increased PFC glucose metabolism 24-hours post-ketamine.
“Convergent data show increased PFC glucose metabolism 24-hours post-ketamine 125,126 , increased fMRI PFC activations acutely (during infusion itself) 127 , and decreased limbic responses to angry (relative to happy) faces among ketamine responders 128 .”
From Neuroplasticity in cognitive and psychological mechanisms of depression: an integrative model (2020) · cites this paper as [125]
The Abstract reports increased prefrontal cortex glucose uptake after ketamine, supporting that part of the claim. The Introduction and Imaging Procedures place the post-ketamine PET measurement about 45–60 minutes after administration, not 24 hours later; the paper therefore does not support the stated timing. Page numbers are unavailable in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measured
Antidepressant outcomes following ketamine treatment correlate well with PFC activation.
“antidepressant outcomes following ketamine treatment correlate well with PFC activation (117, 118)”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [117]
It is possible to activate cortical circuits to produce antidepressant responses without inducing dissociative effects.
“demonstrating that it is possible to activate cortical circuits to produce antidepressant responses without inducing dissociative effects”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [117]
In patients treated with ketamine, floating sensations did not correlate with PFC activation as measured by 18F-PET.
“In patients treated with ketamine, floating sensations did not correlate with PFC activation as measured by 18F-PET”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [117]

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Ketamine ameliorates depressive-like behaviors in mice through increasing glucose uptake regulated by the ERK/GLUT3 signaling pathway
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Beyond NMDA Receptors: A Narrative Review of Ketamine’s Rapid and Multifaceted Mechanisms in Depression Treatment
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Right dorsolateral prefrontal cortex volumetric reduction is associated with antidepressant effect of low-dose ketamine infusion: A randomized, double-blind, midazolam-controlled PET-MRI clinical trial
Li, W., Chen, L., Su, T., Li, C., Lin, W., Wu, H.-J., Tsai, S., Bai, Y., Tu, P., & Chen, M. (2023) · Journal of Affective Disorders · doi:10.1016/j.jad.2023.05.024 · Cited by 7 · see citing works
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Antidepressant and antisuicidal effects of ketamine on the functional connectivity of prefrontal cortex-related circuits in treatment-resistant depression: A double-blind, placebo-controlled, randomized, longitudinal resting fMRI study
Chen, M.-H., Lin, W.-C., Tu, P.-C., Li, C.-T., Bai, Y.-M., Tsai, S.-J., & Su, T.-P. (2019) · Journal of Affective Disorders · doi:10.1016/j.jad.2019.08.022 · Cited by 78 · see citing works
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Persistent antidepressant effect of low-dose ketamine and activation in the supplementary motor area and anterior cingulate cortex in treatment-resistant depression: A randomized control study
Chen, M.-H., Li, C.-T., Lin, W.-C., Hong, C.-J., Tu, P.-C., Bai, Y.-M., Cheng, C.-M., & Su, T.-P. (2018) · Journal of Affective Disorders · doi:10.1016/j.jad.2017.09.008 · Cited by 63 · see citing works
Self-citation
T159. Effect of Ketamine on Prefrontal Cortex Excitability in Treatment Resistant Depression
Selvaraj, S., Ramakrishnan, N., Murphy, N., Durkin, K., Selek, S., Soares, J. C., & Cho, R. Y. (2018) · Biological Psychiatry · doi:10.1016/j.biopsych.2018.02.496

Authors: Li, C., Chen, M., Lin, W., Hong, C., Yang, B., Liu, R., Tu, P., & Su, T.
Affiliations: Taipei Veterans General Hospital (TW)
Corresponding author: Su, Tung‐Ping
ORCID: Li, Cheng‐Ta
Chen, Mu‐Hong
Lin, Wei‐Chen
Yang, Bang‐Hung
Tu, Pei‐Chi
Su, Tung‐Ping
Venue: Human Brain Mapping
Publisher: Wiley
Published: 2016-01-29
Volume: 37
Issue: 3
Pages: 1080-1090
ISSN: 1065-9471 (ISSN-L)
1097-0193
DOI: 10.1002/hbm.23085
PMC: PMC6867460
OpenAlex: W2254316248
Cited by: 152
References: 42
Citations by year: 2026: 10 · 2025: 14 · 2024: 17 · 2023: 17 · 2022: 17 · 2021: 19 · 2020: 19 · 2019: 11 · 2018: 15 · 2017: 8 · 2016: 5
FWCI: 10.51
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Human Brain Mapping (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Ministry of Science and Technology, Taiwan (102‐2314‐B‐010‐060, 103‐2314‐B‐075‐072‐MY3, 103‐2325‐B‐039‐005, 104‐2325‐B‐039‐004)
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: low-dose ketamine, treatment-resistant depression, prefrontal cortex, amygdala, glucose metabolism, glutamatergic neurotransmission, antidepressant mechanism, FDG-PET, antidepressant response, dose-response relationship
MeSH terms: Adult, Amygdala, Antidepressive Agents, Major Depressive Disorder, Dose-Response Relationship, Drug, Double-Blind Method, Female, Humans, Ketamine, Male, Middle Aged, Psychiatric Status Rating Scales, Linear Models, Prefrontal Cortex, Excitatory Amino Acid Antagonists, Glutamic Acid, Radiopharmaceuticals, Fluorodeoxyglucose F18, Positron-Emission Tomography, Depressive Disorder, Treatment-Resistant

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The effects of low‐dose ketamine on the prefrontal cortex and amygdala in treatment‐resistant depression: A randomized controlled study

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