A historical review of antidepressant effects of ketamine and its enantiomers

Wang, Yan; Chang, Lijia; Hashimoto, Kenji

doi:10.1016/j.pbb.2020.172870

Cited by 128 publications

(89 citation statements)

References 126 publications

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“…In this study, increased glutamatergic transmission induced by ketamine application was discussed as a reason for induction of BDNF release (Duman et al 2019 ; Lepack et al 2014 ). However, the molecular mechanisms underlying action of ketamine are not well understood (Lester et al 2012 ; Wei et al 2020 ). Therefore, it is possible that the ketamine-induced BDNF release acts via different mechanisms than glutamate-induced release.…”

Section: Molecular Mechanisms Underlying Release Of Bdnfmentioning

confidence: 99%

The physiology of regulated BDNF release

2020

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The neurotrophic factor BDNF is an important regulator for the development of brain circuits, for synaptic and neuronal network plasticity, as well as for neuroregeneration and neuroprotection. Up- and downregulations of BDNF levels in human blood and tissue are associated with, e.g., neurodegenerative, neurological, or even cardiovascular diseases. The changes in BDNF concentration are caused by altered dynamics in BDNF expression and release. To understand the relevance of major variations of BDNF levels, detailed knowledge regarding physiological and pathophysiological stimuli affecting intra- and extracellular BDNF concentration is important. Most work addressing the molecular and cellular regulation of BDNF expression and release have been performed in neuronal preparations. Therefore, this review will summarize the stimuli inducing release of BDNF, as well as molecular mechanisms regulating the efficacy of BDNF release, with a focus on cells originating from the brain. Further, we will discuss the current knowledge about the distinct stimuli eliciting regulated release of BDNF under physiological conditions.

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Section: Molecular Mechanisms Underlying Release Of Bdnfmentioning

confidence: 99%

The physiology of regulated BDNF release

2020

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“…The N-methyl-D-aspartate receptor (NMDAR) antagonist ketamine (KET) is reported to produce a rapid-onset and sustained antidepressant response [27]. The clinical antidepressant effects of KET were first reported over a decade ago [28]. A single intravenous infusion of sub-anesthetic dose of KET produced rapid antidepressant effect (within hours) that was sustained for up to a week even in patients with refractory depression [29].…”

Section: Introductionmentioning

confidence: 99%

Assessment of Ketamine and its Enantiomers in an Organophosphate-Based Rat Model for Features of Gulf War Illness

Zhu

Hawkins

Phillips

et al. 2020

IJERPH

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Approximately 33% of U.S. soldiers from the first Gulf War suffer from a multi-system disorder known as the Gulf War Illness (GWI). GW veterans suffer from a cluster of symptoms that prominently include fatigue and can include mood-related symptoms. Compared to traditional antidepressants, ketamine (KET) produces a fast-onset and long-lasting antidepressant response, but assessments of KET for GWI-related depression are lacking. The etiology of GWI is multi-factorial and exposure to organophosphates (OP) during deployment is one of the factors underlying GWI development. Here, male Sprague-Dawley rats were repeatedly exposed to an OP DFP and three months later these rats, when assessed on a battery of rodent behavioral assays, displayed signs consistent with aspects of GWI characteristics. When treated with a sub-anesthetic dose of KET (3, 5, or 10 mg/kg, i.p.), DFP-treated rats exhibited a significant improvement in immobility time, open-arm exploration, and sucrose consumption as early as 1 h and much of these effects persisted at 24-h post-KET injection. KET’s stereoisomers, R-KET and S-KET, also exhibited such effects in DFP rats, with R-KET being the more potent isomer. Our studies provide a starting point for further assessment of KET for GWI depression.

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“…mTORC1 stimulation controls synaptic protein translation such as postsynaptic density protein-95 kDa (PSD-95), alpha-amino-3-hydroxy-methyl-5-4-isoxazole propionic acid (AMPA) receptor subunits 1 (GluA1), and synapsin, which are essential for spinogenesis and synaptogenesis ( Abdallah et al, 2016 ). Notably, esketamine was approved for adults with treatment-resistant MDD ( Wei et al, 2020 ). A study by Brachman et al (2016) has provided groundbreaking evidence that ketamine is also effective as a prophylactic agent against stress-induced depressive-like behavior, opening novel perspectives for the design of strategies to prevent MDD.…”

Section: Introductionmentioning

confidence: 99%

Ketamine, but not guanosine, as a prophylactic agent against corticosterone-induced depressive-like behavior: Possible role of long-lasting pro-synaptogenic signaling pathway

Camargo

Dalmagro

Souza

et al. 2020

Experimental Neurology

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Ketamine has been reported to exert a prophylactic effect against stress-induced depressive-like behavior by modulating the guanosine-based purinergic system. However, the molecular pathways underlying its prophylactic effect and whether guanosine also elicits a similar effect remain to be determined. Here, we investigated the prophylactic effect of ketamine and guanosine against corticosterone (CORT – 20 mg/kg, p.o.)-induced depressive-like behavior in mice. Furthermore, we characterized if the prophylactic response may be associated with mTORC1-driven signaling in the hippocampus and prefrontal cortex. A single administration of ketamine (5 mg/kg, i.p.), but not guanosine (1 or 5 mg/kg, p.o.), given 1 week before the pharmacological stress prevented CORT-induced depressive-like behavior in the tail suspension test (TST) and splash test (SPT). Fluoxetine treatment for 3 weeks did not prevent CORT-induced behavioral effects. A single administration of subthreshold doses of ketamine (1 mg/kg, i.p.) plus guanosine (5 mg/kg, p.o.) partially prevented the CORT-induced depressive-like behavior in the SPT. Additionally, CORT reduced Akt (Ser 473 ) and GSK-3β (Ser 9 ) phosphorylation and PSD-95, GluA1, and synapsin immunocontent in the hippocampus, but not in the prefrontal cortex. No alterations on mTORC1/p70S6K immunocontent were found in both regions in any experimental group. CORT-induced reductions on PSD-95, GluA1, and synapsin immunocontent were prevented only by ketamine treatment. Collectively, these findings suggest that ketamine, but not guanosine, exerts a prophylactic effect against depressive-like behavior, an effect associated with the stimulation of long-lasting pro-synaptogenic signaling in the hippocampus.

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A historical review of antidepressant effects of ketamine and its enantiomers

Cited by 128 publications

References 126 publications

The physiology of regulated BDNF release

The physiology of regulated BDNF release

Assessment of Ketamine and its Enantiomers in an Organophosphate-Based Rat Model for Features of Gulf War Illness

Ketamine, but not guanosine, as a prophylactic agent against corticosterone-induced depressive-like behavior: Possible role of long-lasting pro-synaptogenic signaling pathway

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