The interactive effects of ketamine and magnesium upon depressive-like pathology

Approximately one-third of patients with major depressive disorders (MDDs) are resistant to current treatment methods, and the majority of cases relapse at some point during therapy. This has resulted in novel treatments being adopted, including subanesthetic doses of ketamine, which affects aberran...

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Bibliographic Details
Published in:Neuropsychiatric disease and treatment 2016, Vol.12, p.2049-2056
Main Authors: Razmjou, Sara, Litteljohn, Darcy, Rudyk, Chris, Syed, Shuaib, Clarke, Melanie, Pentz, Rowan, Dwyer, Zach, Hayley, Shawn
Format: Article
Language:English
Subjects:
Animal cognition
Anxiety
Behavior
Brain
Brain-derived neurotrophic factor
Depression, Mental
Dosage
Drug therapy
Ketamine
Laboratory animals
Magnesium in the body
Mental depression
Neurotrophic factors
Original Research
Psychiatry
Swimming
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Summary:Approximately one-third of patients with major depressive disorders (MDDs) are resistant to current treatment methods, and the majority of cases relapse at some point during therapy. This has resulted in novel treatments being adopted, including subanesthetic doses of ketamine, which affects aberrant neuroplastic circuits, glutamatergic signaling, and the production of brain-derived neurotrophic factor. Ketamine rapidly relieves depressive symptoms in treatment-resistant major depressive disorder patients with effects that last for up to 2 weeks even after a single administration. However, it is also a drug with an abusive potential and can have marked side effects. Hence, this study aimed at enhancing the antidepressant-like effects of ketamine (allowing for lower dosing regimens) by coadministering magnesium hydroaspartate (Mg(2+) normally affects the same receptors as ketamine) and also assessed whether an Mg(2+)-deficient diet would modify the impact of ketamine. It was found that a single 15 mg/kg dose of ketamine did indeed induce rapid antidepressant-like effects in the forced swim test but did not affect brain levels of the brain-derived neurotrophic factor. Contrary to our hypothesis, magnesium administration or deficiency did not influence the impact of ketamine on these outcomes. Thus, these data do not support the use of magnesium as an adjunct agent and instead suggest that further research involving other antidepressant and animal models is required to confirm the present findings.
ISSN:1176-6328
1178-2021
1178-2021
DOI:10.2147/NDT.S111131