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Trial · NCT04977674

Glutamate and Opioid Mechanisms of Antidepressant Response to Ketamine

NCT04977674, Early phase 1, Completed, King's College London

3 sourcestrials-2026-11-12-0.4.0

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ConductScience Library. Glutamate and Opioid Mechanisms of Antidepressant Response to Ketamine. Trials, record NCT04977674. Release trials-2026-11-12-0.4.0, 12 Nov 2026. https://conductscience.org/library/trials/NCT04977674

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Trial

As registered on ClinicalTrials.gov, in the graph's capture of the registry.

Title
Glutamate and Opioid Mechanisms of Antidepressant Response to Ketamine
NCT number
NCT04977674
Status
Completed
Phases
Early phase 1
Enrollment
27 participants, actual
Lead sponsor
King's College London
Conditions
Depressive Disorder, Treatment-Resistant
Interventions
Naltrexone, Placebo, Ketamine
First posted
2021-07-27
Last updated
2023-03-02

Source ClinicalTrials.gov

Registered outcomes3

Each outcome the trial registered, primary first, in ClinicalTrials.gov's words.

ListOutcomeTime frameDescription
PrimaryChange in GlutamateChanges will be in the same session comparing the ketamine infusion period to the pre-ketamine infusion baseline
Compare changes in glutamate and GLX (glutamate +glutamine), referenced to total creatine (tCr), during ketamine infusion as measured by functional magnetic resonance spectroscopy (1H-fMRS) for naltrexone versus placebo pre-treatment conditions. Hypothesis: There will be a significant increase in glutamate measures during ketamine administration compared to a resting baseline condition in a medial prefrontal cortex (mPFC) /anterior cingulate cortex (ACC) region. Pre-treatment with naltrexone will attenuate this increase.
SecondaryChange in Resting State Functional ConnectivityChanges will be in the same session comparing post-infusion (immediately after ketamine infusion) to the pre-ketamine infusion baseline
Compare changes in functional connectivity as measured by resting state-fMRI post-ketamine administration for naltrexone versus placebo pre-treatment conditions. Hypotheses: 1. Ketamine administration will lead to significant reductions in functional brain connectivity between the subgenual anterior cingulate cortex (sgACC), default mode network (DMN) regions of interest (mPFC and posterior cingulate cortex (PCC)), thalamus, insula and ventral tegmental area (VTA) compared to a resting baseline condition. Pre-treatment with naltrexone will attenuate these reductions. 2. Ketamine administration will lead to a significant increase in functional brain connectivity between the sgACC and dorsolateral prefrontal cortex (DLPFC) compared to a resting baseline condition. Pre-treatment with naltrexone will attenuate this increase.
SecondaryChange in Cerebral Blood FlowChanges will be in the same session comparing data collected 30 minutes after the ketamine infusion commences to the pre-ketamine infusion baseline
Compare changes in cerebral blood flow during ketamine infusion as measured by arterial spin labelling (ASL) for naltrexone versus placebo pre-treatment conditions. Hypothesis: Ketamine administration will lead to a significant increase in CBF in sgACC, pregenual ACC (pgACC), dorsal ACC (dACC) and thalamus regions of interest compared to a resting baseline condition. Pre-treatment with naltrexone will attenuate these increases.

Outcomes0

Each outcome the trial posted results for, in ClinicalTrials.gov's words.

None in this release.

Results by group0

Each measurement the trial posted, group by group, in the words and numbers it posted.

None in this release.

Participant flow0

How many started, completed or left each group, period by period.

None in this release.

Adverse events0

Each adverse event the trial posted, group by group: the participants affected out of those at risk.

None in this release.

Adverse event totals0

The totals the trial posted for each group.

None in this release.

Papers1

The papers the trial lists on ClinicalTrials.gov.

PMIDListed as
40707608DERIVED

Source PubMed

Grants0

The grants NIH RePORTER links to the trial, newest funded first: NIH's, and some of AHRQ's, CDC's, FDA's and VA's. Each shows its title, principal investigators, organization and funder in its newest year.

None in this release.

Trial comparisons0

Comparisons of the trial's two groups, calculated by ConductScience from the counts it posted.

None in this release.

Tests0

The ConductCognition tests this trial's registered outcomes name, as ScienceGraph matched them in trial-tests-2026-11-12-0.2.1.

None in this release.

Source

Release
trials-2026-11-12-0.4.0
Release manifest SHA-256
0f4a8d8c48aee2a7573ae0fa94ecbeab70c1adbe449bbc95c424bc7d3e97b9d4
Registry capture
2026-11-12
Results copy, AACT
2026-03-23
NIH clinical studies file
2026-11-13

Source ClinicalTrials.gov

Sources 3

  • ClinicalTrials.gov's posted results, through CTTI's AACTFreely available. Acknowledgement requested
  • ClinicalTrials.govNone stated
  • NIH RePORTER's clinical studies and project filesPublic domain
Each source's terms
  • ClinicalTrials.gov's posted results, through CTTI's AACTClinicalTrials.gov data via Aggregate Analysis of ClinicalTrials.gov (AACT), CTTI. CTTI makes its materials freely available and requests acknowledgement. https://aact.ctti-clinicaltrials.org/documentation/299
  • ClinicalTrials.govnone stated
  • NIH RePORTER's clinical studies and project filesPublic domain (NIH RePORTER)

ClinicalTrials.gov's data carry an international copyright outside the United States: https://clinicaltrials.gov/about-site/terms-conditions.

For software

Read this trial from software.

The record and each of its lists are JSON, twenty rows a page. No key.

GET https://conductscience.org/api/trials/v1/NCT04977674

GET https://conductscience.org/api/trials/v1/NCT04977674/registered