Chronic ketamine use increases serum levels of brain-derived neurotrophic factor

Ricci, Valerio; Martinotti, Giovanni; Gelfo, Francesca; Tonioni, Federico; Caltagirone, Carlo; Bria, Pietro; Angelucci, Francesco

doi:10.1007/s00213-010-2121-3

Cited by 58 publications

(45 citation statements)

References 54 publications

(44 reference statements)

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“…With regards to the neurochemical effects underlying the antidepressive effects of ketamine, chronic ketamine intake is associated with increases in serum BDNF in humans (Ricci et al, 2011). Although one report in adult rats and mice claimed that ketamine showed a transient effect (at 50 mg/kg) in forced swim and tail suspension tests without any persistent antidepressant effect (Popik et al, 2008), many preclinical studies have recently focused on understanding the molecular mechanisms underlying the rapid-onset prolonged antidepressant effects.…”

Section: F N-methyl-d-aspartate Receptor Antagonistsmentioning

confidence: 99%

Mechanisms of Action and Persistent Neuroplasticity by Drugs of Abuse

Korpi¹,

Hollander²,

Farooq

et al. 2015

Pharmacol Rev

123

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Section: F N-methyl-d-aspartate Receptor Antagonistsmentioning

confidence: 99%

Mechanisms of Action and Persistent Neuroplasticity by Drugs of Abuse

Korpi¹,

Hollander²,

Farooq

et al. 2015

Pharmacol Rev

123

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“…Fourthly, according to previous studies, ketamine has a complex pharmacological profile including glutamatergic, monoaminergic, and GABA-ergic activity [54][55][56][57][58]. Thus physical damages caused by ketamine may not be limited to a single mechanism, such as NMDA antagonism.…”

Section: Perspectivesmentioning

confidence: 99%

Zebrafish as a New Platform Used in Exploration of Ketamine-Induced Neurodevelopmental Toxicity

Ruan¹

2015

J Clin Exp Pathol

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We have modified the abstract as 'Previous studies have already found out that commonly used anesthetic, ketamine, has toxic effects on neurodevelopment. Unlike most rodent models just focusing on neuronal apoptosis caused by ketamine, early stages of neuron development abnormality in zebrafish can be assessed in vivo because of the transparent embryos and larve. And also thanks to its cost-efficiency and quick reproduction, large-scale behavior analyses and gene screens can be conducted in zebrafish. Besides, the whole genome of zebrafish has already been sequenced and its gene functions are highly conserved during evolution, which makes the experiments more reliable on zebrafish model. So Zebrafish has obvious advantages in the researches of ketamine neurotoxicity over the conventional animal models (such as mice). Within this paper we illuminate how we can use this model to study ketamine neurotoxicity. In the future, along with more advanced genetic technologies joining this platform will not only make up for conventional models to deeply understand neurodevelopmental toxicity of ketamine, but also might provide the unique insight to the field of neurodevelopment and neurotoxicity impaired by other drugs

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“…The fact that increased intracellular glutamate release may activate AMPA receptor and this, in turn, may upregulate BDNF gene expression is certainly a plausible hypothesis and is not in contrast with our interpretation. The authors themselves acknowledge that the possibility that glutamate activates AMPA [instead of N-methyl-D-aspartate (NMDA)] receptors is caused by (or linked to) ketamine's antagonist action at NMDA receptor which we proposed as the basic mechanism (Ricci et al 2011). The activation of AMPA receptors plasticity pathways has also been proposed to play a critical role in ketamine's rapid antidepressant effect.…”

mentioning

confidence: 99%