Exploiting N-Methyl-D-Aspartate Channel Blockade for a Rapid Antidepressant Response in Major Depressive Disorder

University of Ottawa Institute of Mental Health Research, Mood Disorders Research, Ottawa, Canada. Electronic address: .
Biological psychiatry (Impact Factor: 10.26). 08/2013; 74(4):238-9. DOI: 10.1016/j.biopsych.2013.05.029
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    European neuropsychopharmacology: the journal of the European College of Neuropsychopharmacology 01/2015; 25(2). DOI:10.1016/j.euroneuro.2014.12.004 · 4.37 Impact Factor
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    ABSTRACT: Ketamine, a rapid-acting antidepressant and anti-suicidal agent, is thought to increase brain monoamine levels by enhancing monoamine release or inhibiting presynaptic monoamine-reuptake. Here we present two female inpatients suffering from treatment-resistant depression with recurrent severe suicidal crises receiving a combination of intravenous S-ketamine and oral tranylcypromine, which is a well-known irreversible monoamine oxidase(MAO) inhibitor. Since inhibition of monoamine-reuptake with concurrent blockade of MAO might trigger sympathomimetic crisis, this combination is considered hazardous. Nonetheless, cardiovascular parameters remained stable in both patients, while good anti-suicidal effects were observed. Hence, we put serious doubt on whether monoamine-reuptake inhibition is a relevant pharmacological effect of ketamine in humans. Copyright © 2015 Elsevier B.V. and ECNP. All rights reserved.
    European neuropsychopharmacology: the journal of the European College of Neuropsychopharmacology 08/2015; DOI:10.1016/j.euroneuro.2015.07.021 · 4.37 Impact Factor