Ketamine-induced changes in plasma brain-derived neurotrophic factor (BDNF) levels are associated with the resting-state functional connectivity of the prefrontal cortex

Woelfer, Marie; Meng, Long; Čolić, Lejla; Liebe, Thomas; Di, Xin; Biswal, Bharat B.; Murrough, James W.; Leßmann, Volkmar; Brigadski, Tanja; Walter, Martin

doi:10.1080/15622975.2019.1679391

Cited by 48 publications

(30 citation statements)

References 105 publications

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“…This line of thinking is supported by recent findings with ketamine and ayahuasca (containing the psychedelic DMT) demonstrating increased serum BDNF levels 24 and 48 h after a single (high) dose, respectively, compared to placebo, which was related to fast antidepressant actions. 21 , 24 , 25 …”

Section: Discussionmentioning

confidence: 99%

Low Doses of LSD Acutely Increase BDNF Blood Plasma Levels in Healthy Volunteers

Hutten

Mason

Dolder

et al. 2020

ACS Pharmacol. Transl. Sci.

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Despite preclinical evidence for psychedelic-induced neuroplasticity, confirmation in humans is grossly lacking. Given the increased interest in using low doses of psychedelics for psychiatric indications and the importance of neuroplasticity in the therapeutic response, this placebo-controlled within-subject study investigated the effect of single low doses of LSD (5, 10, and 20 μg) on circulating BDNF levels in healthy volunteers. Blood samples were collected every 2 h over 6 h, and BDNF levels were determined afterward in blood plasma using ELISA. The findings demonstrated an increase in BDNF blood plasma levels at 4 h (5 μg) and 6 h (5 and 20 μg) compared to that for the placebo. The finding that LSD acutely increases BDNF levels warrants studies in patient populations.

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Section: Discussionmentioning

confidence: 99%

Low Doses of LSD Acutely Increase BDNF Blood Plasma Levels in Healthy Volunteers

Hutten

Mason

Dolder

et al. 2020

ACS Pharmacol. Transl. Sci.

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show abstract

“…This is evidenced by a meta-analysis 86 of 20 studies demonstrating increasing peripheral BDNF levels over the course of treatment with traditional antidepressants. A neuroimaging study 87 showed an association between change in resting state function connectivity, reflecting enhanced synaptic plasticity, and peripheral BDNF levels following ketamine administration in participants without MDD. Interestingly, changes in resting state function connectivity at 24 hours were only seen in participants that had increased BDNF levels at 24 hours as well.…”

Section: Resultsmentioning

confidence: 99%

Retracing our steps to understand ketamine in depression: A focused review of hypothesized mechanisms of action

Irwin

VandenBerg

2021

Mental Health Clinician

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Introduction MDD represents a significant burden worldwide, and while a number of approved treatments exist, there are high rates of treatment resistance and refractoriness. Ketamine, an N-methyl-d-aspartate receptor (NMDAR) antagonist, is a novel, rapid-acting antidepressant, however the mechanisms underlying the efficacy of ketamine are not well understood and many other mechanisms outside of NMDAR antagonism have been postulated based on preclinical data. This focused review aims to present a summary of the proposed mechanisms of action by which ketamine functions in depressive disorders supported by preclinical data and clinical studies in humans. Methods A literature search was completed using the PubMed and Google Scholar databases. Results were limited to clinical trials and case studies in humans that were published in English. The findings were used to compile this article. Results The antidepressant effects associated with ketamine are mediated via a complex interplay of mechanisms; key steps include NMDAR blockade on γ-aminobutyric acid interneurons, glutamate surge, and subsequent activation and upregulation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor. Discussion Coadministration of ketamine for MDD with other psychotropic agents, for example benzodiazepines, may attenuate antidepressant effects. Limited evidence exists for these effects and should be evaluated on a case-by-case basis.

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“…The interplay between LSNs and the cerebellum at rest or during task fMRI are shown to be impaired in several psychiatric disorders, and in MDD specifically ( Miquel et al, 2019 , Depping et al, 2018 ). Studies have also reported that the cerebellum and cortico-cerebellar circuitries are modulated by both standard antidepressant medications ( Guo et al, 2013 , Lupo et al, 2019 , Tozzi et al, 2020 , Khalili-Mahani et al, 2015 ) and single ketamine infusion, which is found to disrupt the connectivity within LSNs and cortico-cerebellar loops in HCs and in MDD ( Reed et al, 2018 , Rush et al, 2003 , Woelfer et al, 2019 ). Further, increased levels of plasma brain-derived neurotrophic factor (BDNF) after single ketamine infusion have been linked with functional connectivity decreases between the dmPFC and posterior cerebellum, which suggests that the antidepressant effects of ketamine may be related to neurotrophic processes in these circuitries ( Behan et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Ketamine’s modulation of cerebro-cerebellar circuitry during response inhibition in major depression

Loureiro

Sahib

Vasavada

et al. 2021

NeuroImage: Clinical

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Highlights Ketamine modulates cerebellar connectivity during response inhibition in depression. Cerebellar–frontoparietal/sensory connectivity decreases in ketamine remitters. Cerebellar-frontoparietal/salience connectivity predicts treatment outcome. Cerebro-cerebellar loops serve as treatment biomarkers in major depression.

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Ketamine-induced changes in plasma brain-derived neurotrophic factor (BDNF) levels are associated with the resting-state functional connectivity of the prefrontal cortex

Cited by 48 publications

References 105 publications

Low Doses of LSD Acutely Increase BDNF Blood Plasma Levels in Healthy Volunteers

Low Doses of LSD Acutely Increase BDNF Blood Plasma Levels in Healthy Volunteers

Retracing our steps to understand ketamine in depression: A focused review of hypothesized mechanisms of action

Ketamine’s modulation of cerebro-cerebellar circuitry during response inhibition in major depression

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