Effect of the multimodal acting antidepressant vortioxetine on rat hippocampal plasticity and recognition memory

Bétry, Cécile; Etiévant, Adeline; Pehrson, Alan L.; Sanchéz, Connie; Haddjeri, Nasser

doi:10.1016/j.pnpbp.2014.12.002

Cited by 44 publications

(32 citation statements)

References 75 publications

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“…Similarly, after chronic dosing, vortioxetine activates neuronal plasticity related genes, improves visual spatial memory deficits, and shows antidepressant-like activity in 12 months old mice, whereas fluoxetine has no effects on any of these measures in old mice [76]. Vortioxetine also increases cell proliferation in the hippocampal dentate gyrus faster than fluoxetine (3 days for vortioxetine compared to 10 days for fluoxetine) [77] in rats, and produces a larger degree of dendritic branching than fluoxetine after two weeks of dosing in mice [78].…”

Section: Vortioxetinementioning

confidence: 97%

Emerging mechanisms and treatments for depression beyond SSRIs and SNRIs

Dale

Bang‐Andersen

Sanchéz

2015

Biochemical Pharmacology

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194

108

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The monoamine hypothesis has been the prevailing hypothesis of depression over the last several decades. It states that depression is associated with reduced monoamine function. Hence efforts to increase monoamine transmission by inhibiting serotonin (5-HT) and norepinephrine (NE) transporters has been a central theme in depression research since the 1960s. The selective 5-HT reuptake inhibitors (SSRIs) and 5-HT and NE reuptake inhibitors (SNRIs) that have emerged from this line of research are currently first line treatment options for major depressive disorder (MDD). One of the recent trends in antidepressant research has been to refine monoaminergic mechanisms by targeting monoaminergic receptors and additional transporters (e.g. with multimodal drugs and triple re-uptake inhibitors) or by adding atypical antipsychotics to SSRI or SNRI treatment. In addition, several other hypotheses of depression have been brought forward in pre-clinical and clinical research based on biological hallmarks of the disease and efficacy of pharmacological interventions. A central strategy has been to target glutamate receptors (for example, with intravenous infusions of the N-methyl-d-aspartate (NMDA) receptor antagonist ketamine). Other strategies have been based on modulation of cholinergic and γ-aminobutyric acid (GABA)ergic transmission, neuronal plasticity, stress/hypothalamic pituitary adrenal(HPA)-axis, the reward system and neuroinflammation. Here we review the pharmacological profiles of compounds that derived from these strategies and have been recently tested in clinical trials with published results. In addition, we discuss putative treatments for depression that are being investigated at the preclinical level and outline future directions for antidepressant research.

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Section: Vortioxetinementioning

confidence: 97%

Emerging mechanisms and treatments for depression beyond SSRIs and SNRIs

Dale

Bang‐Andersen

Sanchéz

2015

Biochemical Pharmacology

Self Cite

194

108

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“…In this study, a single dose of most of the drugs was used. Thus, the dosage and timing of drugs used here were determined referring to our and others’ previous studies where the drugs affected behaviors and/or neurotransmitter release (Moser et al, 1996; Ago et al, 2006a, 2006b, 2007, 2011b, 2013, 2015; Collins et al, 2010; Jones et al, 2010; Hiramatsu et al, 2013; Bétry et al, 2015; Hasebe et al, 2015). To induce METH-induced behavioral sensitization, mice were injected with METH (1 mg/kg) once daily for 7 days, as previously described (Ago et al, 2006b, 2007, 2012).…”

Section: Methodsmentioning

confidence: 99%

Role of prefrontal serotonergic and dopaminergic systems in encounter-induced hyperactivity in methamphetamine-sensitized mice

Tanaka

Ago

Umehara

et al. 2016

IJNPPY

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Background:Isolation-reared mice show social encounter-induced hyperactivity with activation of prefrontal serotonergic and dopaminergic systems, but it is not known whether this stress response is observed in other pathological conditions. Here we examined whether the social encounter stimulation induces abnormal behavior during withdrawal in chronic methamphetamine-treated mice.Methods:To induce methamphetamine-induced behavioral sensitization, male mice were injected with methamphetamine (1 mg/kg) once daily for 7 days.Results:The encounter with an intruder elicited hyperactivity 24 h after the last injection of methamphetamine in methamphetamine-sensitized mice. This response was observed even as long as 2 weeks after withdrawal of methamphetamine. The encounter increased c-Fos expression in the prefrontal cortex, dorsal raphe nucleus and ventral tegmental area in methamphetamine-sensitized mice, while it did not in control mice. Furthermore, the encounter increased extracellular serotonin (5-HT) and dopamine, but not noradrenaline, levels in the prefrontal cortex in methamphetamine-sensitized mice. Local injection of 5,7-dihydroxytryptamine and 6-hydroxydopamine into the prefrontal cortex attenuated encounter-induced hyperactivity in methamphetamine-sensitized mice and it markedly decreased prefrontal 5-HT and dopamine levels, respectively. Pharmacological analysis showed that the encounter-induced hyperactivity is mediated by dopamine D1 receptors and 5-HT2A receptors and attenuated by anxiolytics and antidepressants such as diazepam, osemozotan and selective 5-HT reuptake inhibitors. The effect of paroxetine was blocked by the 5-HT3 receptor antagonist azasetron.Conclusions:The present study shows that psychological stress elicits hyperactivity with activation of prefrontal 5-HT and dopamine systems in methamphetamine-dependent mice and suggests that the abnormal behavior is associated with anxiety and depression.

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“…Also newer compounds, like a multimodal agent vortioxetine, after chronic treatment were shown to increase dendritic length and the number of dendrite intersections as well as to increase cell proliferation, cell survival and stimulate maturation of immature granule cells in the subgranular zone of the dentate gyrus [126]. Moreover, vortioxetine [127] but also other generations of antidepressants like SSRIs (escitalopram) [128] or SNRIs (milnacipran) [129] were found to prevent the effects of stress on hippocampal long term potentiation (LTP), one of the phenomena underlying synaptic plasticity [130]. In the next paragraph we will discuss the role of zinc in the processes related to neural plasticity and then possible interactions between zinc and monoamine-based antidepressants in the context of neural plasticity.…”

Section: Link To Neural Plasticitymentioning

confidence: 99%

Zinc in the Monoaminergic Theory of Depression: Its Relationship to Neural Plasticity

et al. 2017

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Preclinical and clinical studies have demonstrated that zinc possesses antidepressant properties and that it may augment the therapy with conventional, that is, monoamine-based, antidepressants. In this review we aim to discuss the role of zinc in the pathophysiology and treatment of depression with regard to the monoamine hypothesis of the disease. Particular attention will be paid to the recently described zinc-sensing GPR39 receptor as well as aspects of zinc deficiency. Furthermore, an attempt will be made to give a possible explanation of the mechanisms by which zinc interacts with the monoamine system in the context of depression and neural plasticity.

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Effect of the multimodal acting antidepressant vortioxetine on rat hippocampal plasticity and recognition memory

Cited by 44 publications

References 75 publications

Emerging mechanisms and treatments for depression beyond SSRIs and SNRIs

Emerging mechanisms and treatments for depression beyond SSRIs and SNRIs

Role of prefrontal serotonergic and dopaminergic systems in encounter-induced hyperactivity in methamphetamine-sensitized mice

Zinc in the Monoaminergic Theory of Depression: Its Relationship to Neural Plasticity

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