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Ketamine's Actions on Rumination Mechanisms as an Antidepressant

NCT04656886 · Status: COMPLETED · Phase: NA · Type: INTERVENTIONAL · Enrollment: 37

Last updated 2020-12-07

No results posted yet for this study

Summary

Rumination and anhedonia are two of the most common characteristics of depression that persist during remission and are not easily targeted by commonly prescribed antidepressants. Ketamine, an NMDA receptor antagonist, has emerged within the last decade as a potent, fast-acting antidepressant that can significantly improve anhedonia as early as two hours after a single infusion. The brain mechanisms, however, by which ketamine exerts its antidepressant action remain largely unknown. The aim of this study is to examine the early antidepressant action of ketamine, 2h post infusion, in patients who remitted from depression using fMRI. Participants are scanned while performing a personalised, autobiographical, emotional memory task and a monetary reward task. Ketamine is expected to reduce the activation of limbic areas such as the amygdala during emotional memory recall. Increased activations after ketamine are expected in reward processing areas, including striatal regions.

Conditions

  • Remission in Depression

Interventions

DRUG

Intravenous Infusion

Sponsors & Collaborators

Study Design

Allocation
RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
DOUBLE
Model
CROSSOVER

Eligibility

Min Age
18 Years
Max Age
50 Years
Sex
ALL
Healthy Volunteers
Yes

Timeline & Regulatory

Start
2014-09-30
Primary Completion
2018-05-31
Completion
2018-05-31

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Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT04656886 on ClinicalTrials.gov