Vesicular glutamate transporter 1 (VGLUT1)-mediated glutamate release and membrane GluA1 activation is involved in the rapid antidepressant-like effects of scopolamine in mice

Yu, Hanjie; Li, Mengmeng; Zhou, Dongsheng; Lv, Dan; Liao, Qi; Lou, Zhongze; Shen, Mengxin; Wang, Zhen; Li, Ming; Xiao, Xiao; Zhang, Yanhua; Wang, Chuang

doi:10.1016/j.neuropharm.2017.12.028

Cited by 36 publications

(25 citation statements)

References 63 publications

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“…Previous studies have shown that VGluT1 is associated with depression-like behaviors [46] and is involved in rapid antidepressant-like effects. [47] It is therefore possible that the depression-like behaviors in aged mice may be attributed to the decrease in VGluT1 levels in stress-sensitive brain regions. The unaffected VGAT levels could be related to compensatory VGAT expression in other types of inter-neurons.…”

Section: Discussionmentioning

confidence: 99%

Adolescent stress increases depression-like behaviors and alters the excitatory-inhibitory balance in aged mice

Wang

Sun

Liu

et al. 2019

Chinese Medical Journal

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Background:Depression affects approximately 5% of elderly people and its etiology might be related to chronic stress exposure during neurodevelopmental periods. In this study, we examined the effects of adolescent chronic social stress in aged mice on depressive behaviors and the excitatory-inhibitory (E/I) balance in stress-sensitive regions of the brain.Methods:Sixty-four adolescent, male C57BL/6 mice were randomly assigned to either the 7-week (from post-natal days 29 to 77) social instability stress (stress group, n = 32) or normal housing conditions (control group, n = 32). At 15 months of age, 16 mice were randomly selected from each group for a series of behavioral tests, including two depression-related tasks (the sucrose preference test and the tail suspension test). Three days following the last behavioral test, eight mice were randomly selected from each group for immunohistochemical analyses to measure the cell density of parvalbumin (PV+)- and calretinin (CR+)-positive gamma-aminobutyric-acid (GABA)ergic inhibitory inter-neurons, and the expression levels of vesicular transporters of glutamate-1 (VGluT1) and vesicular GABA transporter (VGAT) in three stress-sensitive regions of the brain (the medial pre-frontal cortex [mPFC], hippocampus, and amygdala).Results:Behaviorally, compared with the control group, adolescent chronic stress increased depression-like behaviors as shown in decreased sucrose preference (54.96 ± 1.97% vs. 43.11 ± 2.85%, t(22) = 3.417, P = 0.003) and reduced latency to immobility in the tail suspension test (92.77 ± 25.08 s vs. 33.14 ± 5.95 s, t(25) = 2.394, P = 0.025), but did not affect anxiety-like behaviors and pre-pulse inhibition. At the neurobiologic level, adolescent stress down-regulated PV+, not CR+, inter-neuron density in the mPFC (F(1, 39) = 19.30, P < 0.001), and hippocampus (F(1, 42) = 5.823, P = 0.020) and altered the CR+, not PV+, inter-neuron density in the amygdala (F(1, 28) = 23.16, P < 0.001). The VGluT1/VGAT ratio was decreased in all three regions (all F > 10.09, all P < 0.004), which suggests stress-induced hypoexcitability in these regions.Conclusions:Chronic stress during adolescence increased depression-like behaviors in aged mice, which may be associated with the E/I imbalance in stress-sensitive brain regions.

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Section: Discussionmentioning

confidence: 99%

Adolescent stress increases depression-like behaviors and alters the excitatory-inhibitory balance in aged mice

Wang

Sun

Liu

et al. 2019

Chinese Medical Journal

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“…Long-term antidepressant effects are associated with upregulation of synaptic levels of AMPARs, similar to what occurs during LTP induced in brain slices. Upregulation of AMPAR synaptic expression has been measured in immunoblots from animals within 24 hours after treatment with ketamine and other putative rapid-acting antidepressant drugs (68, 71, 107, 129, 139). Consistent with an increase in synaptic AMPARs being involved in sustained antidepressant actions, administration of NBQX immediately prior to antidepressant behavioral testing—at a time point distant from drug administration—has been shown to prevent expression of the antidepressant actions of both ketamine and ( 2R,6R )-HNK (68, 127).…”

Section: Neurophysiological Mechanisms Underlying Rapid-acting Antidementioning

confidence: 99%

Molecular Pharmacology and Neurobiology of Rapid-Acting Antidepressants

Gould

Zarate

Thompson

2019

Annu. Rev. Pharmacol. Toxicol.

103

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For decades, symptoms of depression have been treated primarily with medications that directly target the monoaminergic brain systems, which typically take weeks to exert measurable effects and months to exert remission of symptoms. Low, subanesthetic doses of (R,S)-ketamine (ketamine) result in the rapid improvement of core depressive symptoms, including mood, anhedonia, and suicidal ideation, occurring within hours following a single administration, with relief from symptoms typically lasting up to a week. The discovery of these actions of ketamine has resulted in a reconceptualization of how depression could be more effectively treated in the future. In this review, we discuss clinical data pertaining to ketamine and other rapid-acting antidepressant drugs, as well as the current state of pharmacological knowledge regarding their mechanism of action. Additionally, we discuss the neurobiological circuits that are engaged by this drug class and that may be targeted by a future generation of medications, for example, hydroxynorketamine; metabotropic glutamate receptor 2/3 antagonists; and N-methyl-D-aspartate, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, and γ-aminobutyric acid receptor modulators.

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“…However, knockdown of BICC1 in the hippocampus protected rats from CUS-induced depressive behavior, and a single acute antidepressant dose of ketamine resulted in rapid BICC1 mRNA downregulation in vivo 14. In addition, scopolamine (25 or 50 mg/kg) treatment significantly reversed the upregulation of BICC1 in the prefrontal cortex of the CUS-induced depressive mice 22. These findings may explain the observation of enhanced levels of serum BICC1 in patients with mood disorders and suggest that the increased levels of BICC1 may be associated not only with the pathophysiology of MDD but also with other types of mood disorders.…”

Section: Discussionmentioning

confidence: 95%

Serum BICC1 levels are significantly different in various mood disorders

Chen

Jiang

et al. 2019

NDT

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PurposeMood disorders are recurrent chronic disorders with fluctuating mood states and energy, and misdiagnosis is common when based solely on clinical interviews because of overlapping symptoms. Because misdiagnosis may lead to inappropriate treatment and poor prognosis, finding an easily implemented objective tool for the discrimination of different mood disorders is very necessary and urgent. However, there has been no accepted objective tool until now. Recently, BICC1 has been identified as a candidate gene relating to major depressive disorder (MDD). Therefore, the aim of this study is to evaluate the ability of serum BICC1 to discriminate between various mood disorders, including MDD and the manic and depressive phases of bipolar disorder, namely bipolar mania (BM) and bipolar depression (BD).Patients and methodsSerum BICC1 levels in drug-free patients with MDD (n=30), BM (n=30), and BD (n=13), and well-matched healthy controls (HC, n=30) were measured with ELISA kits. Pearson correlation analyses were used to analyze the correlations between serum BICC1 levels and clinical information. Receiver operating characteristic (ROC) curve analysis was used to analyze the differential discriminative potential of BICC1 for different mood disorders.ResultsOne-way ANOVA indicated that serum BICC1 levels were significantly increased in all patient groups compared with the HC group and significantly different between each pair of patient groups. Correlation analyses found no relationship between serum BICC1 levels and any clinical variables in any study group. ROC curve analysis showed that serum BICC1 could discriminate among all three mood disorders from each other accurately with fair-to-excellent discriminatory capacity (area under the ROC curve from 0.787 to 1.0).ConclusionThe findings of this preliminary study indicated significant differences in serum BICC1 levels in patients with different mood disorders. This study provides preliminary evidence that serum BICC1 may be regarded as a promising, objective, easy-to-use tool for diagnosing different mood disorders.

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Vesicular glutamate transporter 1 (VGLUT1)-mediated glutamate release and membrane GluA1 activation is involved in the rapid antidepressant-like effects of scopolamine in mice

Cited by 36 publications

References 63 publications

Adolescent stress increases depression-like behaviors and alters the excitatory-inhibitory balance in aged mice

Adolescent stress increases depression-like behaviors and alters the excitatory-inhibitory balance in aged mice

Molecular Pharmacology and Neurobiology of Rapid-Acting Antidepressants

Serum BICC1 levels are significantly different in various mood disorders

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