Journal
MOLECULAR PSYCHIATRY
Volume 23, Issue 4, Pages 824-832Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/mp.2017.58
Keywords
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Funding
- Biostatistical Consulting Core at the School of Medicine, Stony Brook University
- VA National Center for PTSD
- [K01MH092681]
- [K01MH091354]
- [R01MH104512]
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The mechanisms of action of the rapid antidepressant effects of ketamine, an N-methyl-D-aspartate glutamate receptor antagonist, have not been fully elucidated. This study examined the effects of ketamine on ligand binding to a metabotropic glutamatergic receptor (mGluR5) in individuals with major depressive disorder (MDD) and healthy controls. Thirteen healthy and 13 MDD nonsmokers participated in two [C-11] ABP688 positron emission tomography (PET) scans on the same day-before and during intravenous ketamine administration-and a third scan 1 day later. At baseline, significantly lower [C-11] ABP688 binding was detected in the MDD as compared with the control group. We observed a significant ketamine-induced reduction in mGluR5 availability (that is, [C-11] ABP688 binding) in both MDD and control subjects (average of 14 +/- 9% and 19 +/- 22%, respectively; P < 0.01 for both), which persisted 24 h later. There were no differences in ketamine-induced changes between MDD and control groups at either time point (P = 0.8). A significant reduction in depressive symptoms was observed following ketamine administration in the MDD group (P < 0.001), which was associated with the change in binding (P < 0.04) immediately after ketamine. We hypothesize that glutamate released after ketamine administration moderates mGluR5 availability; this change appears to be related to antidepressant efficacy. The sustained decrease in binding may reflect prolonged mGluR5 internalization in response to the glutamate surge.
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