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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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Autores principales: Razmjou, Sara, Litteljohn, Darcy, Rudyk, Chris, Syed, Shuaib, Clarke, Melanie, Pentz, Rowan, Dwyer, Zach, Hayley, Shawn
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5019465/
https://www.ncbi.nlm.nih.gov/pubmed/27660449
http://dx.doi.org/10.2147/NDT.S111131
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author Razmjou, Sara
Litteljohn, Darcy
Rudyk, Chris
Syed, Shuaib
Clarke, Melanie
Pentz, Rowan
Dwyer, Zach
Hayley, Shawn
author_facet Razmjou, Sara
Litteljohn, Darcy
Rudyk, Chris
Syed, Shuaib
Clarke, Melanie
Pentz, Rowan
Dwyer, Zach
Hayley, Shawn
author_sort Razmjou, Sara
collection PubMed
description 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.
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spelling pubmed-50194652016-09-22 The interactive effects of ketamine and magnesium upon depressive-like pathology Razmjou, Sara Litteljohn, Darcy Rudyk, Chris Syed, Shuaib Clarke, Melanie Pentz, Rowan Dwyer, Zach Hayley, Shawn Neuropsychiatr Dis Treat Original Research 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. Dove Medical Press 2016-09-08 /pmc/articles/PMC5019465/ /pubmed/27660449 http://dx.doi.org/10.2147/NDT.S111131 Text en © 2016 Razmjou et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Original Research
Razmjou, Sara
Litteljohn, Darcy
Rudyk, Chris
Syed, Shuaib
Clarke, Melanie
Pentz, Rowan
Dwyer, Zach
Hayley, Shawn
The interactive effects of ketamine and magnesium upon depressive-like pathology
title The interactive effects of ketamine and magnesium upon depressive-like pathology
title_full The interactive effects of ketamine and magnesium upon depressive-like pathology
title_fullStr The interactive effects of ketamine and magnesium upon depressive-like pathology
title_full_unstemmed The interactive effects of ketamine and magnesium upon depressive-like pathology
title_short The interactive effects of ketamine and magnesium upon depressive-like pathology
title_sort interactive effects of ketamine and magnesium upon depressive-like pathology
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5019465/
https://www.ncbi.nlm.nih.gov/pubmed/27660449
http://dx.doi.org/10.2147/NDT.S111131
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